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Textbooks: Cecil Essentials of Medicine, Hospital Medicine Secrets, First Aid for Medical Clerkship Introductory Guide: Primer to the Internal Medicine Clerkship 2nd Edition by Picchioni -------------------------------------------------------------------------------------------------------------------------------------------Common Problems in Internal Medicine Cardiovascular: Acute Coronary Syndromes, Congestive Heart Failure, Valvular Heart Disease, Atrial Fibrillation and Anticoagulation, Hypertension Endocrine: Diabetes Mellitus, Hypothyroidism, Hyperthyroidism, Osteoporosis, Disorders of Calcium Metabolism Hematology: Anemia, Coagulopathies Gastro: Hepatitis, Peptic Ulcer Disease, Gastroesophageal Reflux Disease, Diarrhea and Constipation Oncology: Hematological Malignancy, General Care of the Cancer Patient, Management of Pain Nephrology: Electrolyte Disturbances, Acid-Base Disorders, Acute and Chronic Renal Failure Rheumatology: Rheumatoid Arthritis, Osteoarthritis, Monoarthritides, Polyarthritides Pulmonary: DVT and Pulmonary Embolism, Chronic Bronchitis and Asthma, Emphysema Infectious: Fever of Unknown Origin, Acquired Immune Deficiency Syndrome, Pneumonia, Urinary Tract Infection, Cellulitis, Subacute Bacterial Endocarditis Allergy: Urticaria Neurology: Cerebrovascular Disease, Headache, Dementia and Coma Dermatology: Dermatological Manifestations of Chronic Medical Disease -------------------------------------------------------------------------------------------------------------------------------------------Procedures: NEJM Videos In Clinical Medicine: http://www.nejm.org/multimedia/videosinclinicalmedicine -------------------------------------------------------------------------------------------------------------------------------------------Kaplan Videos (2001) – Board Studying Thoughts from Dr. Conrad Fischer, MD * For USMLE Step 2 (and any exam for that matter), think from the point of view of the question writer. Questions you can expect include “Which of the following is the most likely diagnosis?” seem commonly in Internal Medicine sections, where physicians ponder over the diagnosis for hours. Diagnosis questions account for about 20-30%, more in Internal Medicine, less on Surgery. “Which of the following is the best initial diagnostic test?” or “What would you do first to confirm your diagnosis?” Also, “What is the best diagnostic test” or “What is the most accurate diagnostic test?” Treatment questions follow “Which of the following is the best initial therapy?” Always ask “What is the next best step in the management of this patient?” * What is the problem? Pay attention to the question. If the question asks what is the best initial diagnostic test and you pick the best test (most accurate), you missed the question. If the question asks what is the best initial therapy and you choose the best therapy (most effective), you missed the question. * But you think to yourself, no no no I don’t do this. I won’t make this mistake. But, you do make this mistake because everybody makes this mistake. Examination results show this time and time again. * Answer questions based on what the question-writer is saying, now what you think they mean. * You’re sitting there looking up at that board exam and all you see is a huge exam. You feel scared and all you can think about is how big that exam is. But, if you could find a way to look past the exam and see good and beauty. You could connect with the goodness and beauty that is beyond the exam, which you can’t do right now because all you see is a giant exam. But, if you can connect with the knowledge, the data that you need for the exam and connect it with the beauty and good, great things will happen. * First, the exam will seem much smaller and lighter in the palm of your hands (from William Blake). Second, you will be able to remember the knowledge longer and help someone later on with it, and that is a great good. Third, you will get a better grade anyway and get what you want. If doing well on the exam is your highest aspiration, it will become so painful. Fourth, your trip/voyage/journey will be filled with much more joy. This idea is the analgesic for your studying. -------------------------------------------------------------------------------------------------------------------------------------------How To Succeed In Clerkship – First Aid For The Medicine Clerkship (Stead, Stead, & Kaufman) Be On Time: Team rounds usually begin between 7am and 8am. Give yourself at least 10 minutes per patient for pre-rounding to learn about events that occurred overnight or lab/imaging results. Dress In A Professional Manner: Regardless of what the attending wears. A short white coat should be worn over your professional dress clothes unless it is discouraged (e.g. pediatrics). Act In A Pleasant Manner: The medical rotation is often difficult, stressful, and tiring. Smooth out your experience by being nice to be around. Smile a lot and learn everyone’s name. Don’t be afraid to ask how your resident’s weekend was. If you do not under- stand or disagree with a treatment plan or diagnosis, do not “challenge.” Instead, say “I’m sorry, I don’t quite understand, could you please explain…” Show kindness and compassion toward your patients. Never participate in callous talk about patients.
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Study Notes – Internal Medicine
Take Responsibility: Know everything there is to know about your patients: their history, test results, details about their medical problem, and prognosis. Keep your intern or resident informed of new developments that they might not be aware of, and ask them for any updates you might not be aware of. Assist the team in developing a plan; speak to radiology, consultants, and family. Never give bad news to patients or family members without the assistance of your supervising resident or attending. Respect Patient’s Rights: 1) All patients have the right to have their personal medical information kept private. This means do not discuss the patient’s information with family members without that patient’s consent, and do not discuss any patient in hallways, elevators, or cafeterias. 2) All patients have the right to refuse treatment. This means they can refuse treatment by a specific individual (you, the medical student) or of a specific type (no nasogastric tube). Patients can even refuse life- saving treatment. The only exceptions to this rule are if the patient is deemed to not have the capacity to make decisions or understand situations, in which case a health care proxy should be sought, or if the patient is suicidal or homicidal. 3) All patients should be informed of the right to seek advanced directives on admission. Often, this is done by the admissions staff, in a booklet. If your patient is chronically ill or has a life-threatening illness, address the subject of advanced directives with the assistance of your attending. More Tips: Volunteer, be a team player, be honest, and keep patient information handy. Present In An Organized Manner: “This is a [age]-year-old [gender] with a history of [major history such as HTN, DM, coronary artery disease, CA, etc.] who presented on [date] with [major symptoms, such as cough, fever, and chills] and was found to have [working diagnosis]. [Tests done] showed [results]. Yesterday, the patient [state important changes, new plan, new tests, new medications]. This morning the patient feels [state the patient’s words], and the physical exam is significant for [state major findings]. Plan is [state plan].” -------------------------------------------------------------------------------------------------------------------------------------------Presenting A Chest Radiograph (CXR): 1) Technique: Rotation, anteroposterior (AP) or posteroanterior (PA), penetration, inspiratory effort. 2) Bony structures: Look for rib, clavicle, scapula, and sternum fractures. 3) Airway: Look for tracheal deviation, pneumothorax, and pneumomediastinum. 4) Pleural space: Look for fluid collections, which can represent hemothorax, chylothorax, and pleural effusion. 5) Lung parenchyma: Look for infiltrates and consolidations: These can represent pneumonia, pulmonary contusions, hematoma, or aspiration. The location of an infiltrate can provide a clue to the location of pneumonia: * Obscured right (R) costophrenic angle = Right lower lobe * Obscured left (L) costophrenic angle = Left lower lobe * Obscured R heart border = Right middle lobe * Obscured L heart border = Left upper lobe 6) Mediastinum: Look at size of mediastinum—a widened one (> 8 cm) goes with aortic dissection. Look for enlarged cardiac silhouette (> 1⁄2 thoracic width at base of heart), which may represent congestive heart failure (CHF), cardiomyopathy, or pericardial effusion. 7) Diaphragm: Look for free air under the right hemidiaphragm (suggests perforation). Look for stomach, bowel, or nasogastric tube (NGT) above diaphragm (suggests diaphragmatic rupture). 8) Tubes and lines: * Identify all tubes and lines. * An endotracheal tube should be 2cm above the carina. Common mistake is right bronchus intubation. * A chest tube (and proximal hole) should be in the pleural space (not in the lung parenchyma). * An NGT should be in the stomach and uncoiled. * The tip of a central venous catheter should be in the superior vena cava (not in the right atrium). * The tip of a Swan–Ganz catheter should be in the pulmonary artery. * The tip of a transvenous pacemaker should be in the right atrium. -------------------------------------------------------------------------------------------------------------------------------------------Presenting A Chest Radiograph (Mnemonic Method): Mnemonic: RRR, RIP, ABCDEFGH * Right: patient, procedure, date * Rotation: spinous processes are to line up vertically, equal space between clavicles * Inspiration: should show 8 ribs * Penetration: spinous processes should just be visible through the vertebrae * Airway: carina and tracheal deviation * Bones: look at clavicles, vertebrae, scapula, and ribs for fractures
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Study Notes – Internal Medicine
* Cardiac silhouette: > 1/2 total chest width could be CHF, determine if edges are clear * Diaphragm: elevated or depressed, right should be higher, no air under diaphragm * Effusions: check borders and edges for fluid levels, hemothorax, atelectasis, pneumothorax * Fields: infiltrates, masses, objects, size (large in emphysema, small in chronic bronchitis) * Gadgets: ET tubes, central lines, chest tubes, pacemakers, ECG monitors, mention this after RRR RIP in ICU * Hilum: any masses or disturbances -------------------------------------------------------------------------------------------------------------------------------------------Presenting An Electrocardiogram (ECG): 1) Rate: The rate is [number of] beats per minute (bpm): * The ECG paper is scored so that one big box is 0.20 seconds. These big boxes consist of five little boxes, each of which is 0.04 seconds. * A quick way to calculate rate when the rhythm is regular is the mantra: 300, 150, 100, 75, 60, 50 (= 300 / # large boxes), which is measured as the number of large boxes between two QRS complexes. Therefore, a distance of one large box between two adjacent QRS complexes would be a rate of 300, while a distance of five large boxes between two adjacent QRS complexes would be a rate of 60. * For irregular rhythms, count the number of complexes that occur in a 6-second interval (30 large boxes) and multiply by 10 to get a rate in bpm. 2) Rhythm: The rhythm is [sinus]/[atrial fibrillation]/[atrial flutter] or other: * If p waves are present in all leads and upright in leads I and aVF, then the rhythm is sinus. Lack of p waves suggests a disorganized atrial rhythm, a junctional rhythm, or a ventricular rhythm. A ventricular rhythm (V Fib or V Tach) is an unstable one (could spell imminent death), and you should be getting ready for advanced cardiac life support (ACLS). * Normal sinus rhythm is usually a regular narrow-complex rhythm with each QRS complex preceded by a p wave. 3) Axis: The axis is [normal]/[deviated to the right]/[deviated to the left]: * If I and aVF are both upright or positive, then the axis is normal. * If I is upright and aVF is upside down, then there is left axis deviation (LAD). * If I is upside down and aVF is upright, then there is right axis deviation (RAD). * If I and aVF are both upside down or negative, then there is extreme RAD. 4) Intervals: The [PR]/[QRS] intervals are [normal]/[shortened]/[widened]: * Normal PR interval = 0.12 to 0.20 seconds: * Short PR is associated with Wolff–Parkinson–White syndrome (WPW). * WPW syndrome is characterized by a “delta” wave, or slurred up-stroke of QRS complex. * Long PR interval is associated with heart block of which there are three types: * First-degree block: PR interval > 0.20 seconds (one big box) * Second-degree (Mobitz type I or Wenckebach) block: PR interval lengthens progressively until a QRS is dropped. * Second-degree (Mobitz type II) block: PR interval is constant, but one QRS is dropped at a fixed interval. * Third-degree heart block: Complete AV dissociation Normal QRS interval ≤ 0.12 seconds: * Prolonged QRS is seen when the beat is initiated in the ventricle rather than the sinoatrial node, when there is a bundle branch block, and when the heart is artificially paced with longer QRS intervals. Prolonged QRS is also noted in tricyclic overdose and Wolfe–Parkinson–White syndrome. 5) Wave morphology: A. Ventricular hypertrophy: There [is/is no] [left/right] [ventricular/atrial] hypertrophy: * There are multiple criteria for determining right (RVH) and left ventricular hypertrophy (LVH). Clues for LVH: * RI>15mm, RI,II or aVF >20mm, RaVL>11mm, RV5 or RV6 >26mm, RI +SIII >25mm, R+S in Vlead>45mm, SV1 +RV5 or RV6 >35mm Clues for RVH: * RV1>7mm, SV1<2mm, R/S ratio inV1 >1, RAD of 110deg or more B. Atrial hypertrophy: * Right atrial hypertrophy: tall or peaked p waves in limb or precordial leads * Left atrial hypertrophy: broad or notched p waves in limb leads C. Ischemic changes: There [are/are no] S-T wave [depressions/elevations] or [flattened/inverted] T waves. Presence of Q wave indicates an old infarct. D. Bundle branch block: There [is/is no] [left/right] bundle branch block. Clues: * Presence of RSR’ wave in leads V1-V3 with ST depression and T wave inversion goes with RBBB. * Presence of notched R wave in leads I, aVL, and V4-V6 goes with LBBB.
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11) All patients with coronary artery disease (CAD). in whom TSH cannot reliably to assess thyroid function. and endocrine hyperfunction. influenza. 4) The most common etiologic agent implicated in acute bacterial meningitis in the U. 16) Noninvasive stress testing has the best predictive value for detecting CAD in patients with an intermediate (3080%) pretest likelihood of CAD and is of limited value in patients with very low (< 30%) or very high (> 80%) likelihood of CAD. 20) Community-acquired methicillin-resistant Staphylococcus aureus that is susceptible to clindamycin but resistant to erythromycin should not be treated with clindamycin because of the possibility for induction of resistance. regardless of the blood low-density lipoprotein (LDL) cholesterol level. 5) In the newly diagnosed HIV patient. 15) Angiotensin-converting enzyme inhibitors (or angiotensin receptor blockers) and beta-adrenergic blockers are effective in reducing cardiovascular complications and improving survival in patients with systolic heart failure and are recommended in all patients with no contraindications to these drugs. or gender. 9) The best initial screening test for evaluation of thyroid status is the TSH. 3) In the approach to suspected PE. 14) The single most life-saving treatment strategy in patients with acute ST-elevation myocardial infarction is to rapidly achieve complete reperfusion of the infarct-related artery by mechanical (balloon angioplasty or stenting) or pharmacologic means (thrombolysis). approximately 50% of cases are diagnosed post mortem. DO NOT DISTRIBUTE -4- . and (3) a negative Doppler venous ultrasound of the legs does not exclude the diagnosis of PE. and rising titers suggest worsening disease. 10) The most common presentation of hypogonadism is erectile dysfunction and decreased libido in men and amenorrhea and infertility in women. is Streptococcus pneumoniae. or diabetes should be treated aggressively to reach the LDL-cholesterol target of 100 mg/dL. which applies pressure to surrounding structures. hypertriglyceridemia.S. (2) chest CT can help detect most PEs. elimination of secondary infections. 8) A key concept in evaluating patients with hyperfunctioning endocrine tumors is that biochemical diagnosis should always precede anatomic localization. The one exception is patients with pituitary/hypothalamic dysfunction. hypertension. immunizations against pneumococcal pneumonia. and fasting hyperglycemia. euglycemia. higher titers of complement-fixing antibodies suggest more extensive disease. which results in excessive secretion of a particular anterior pituitary hormone. 18) Patients who present with flaccid paralysis during the summer months should be evaluated for West Nile virus infection. 22) Transmission of Borrelia burgdorferi (the causative agent of Lyme disease) from an infected Ixodes tick to a susceptible human requires the tick to have fed on the human for at least 40 hours. and establishment of therapeutic goals. 13) The goal blood pressure is < 130/80 mmHg in hypertensive subjects with diabetes mellitus and/or chronic kidney disease. 21) In patients with disseminated candidiasis. 12) Diabetics and patients with vascular disease should be treated with a statin lipid-lowering drug to prevent heart disease and stroke. 19) A febrile patient with rash who presents to the emergency department during May to September in the South Atlantic and West South Central states should receive empirical doxycycline therapy for suspected Rocky Mountain spotted fever. Zollo) 1) The treatment of severe sepsis syndrome should be based on efficient resuscitation. and both hepatitis A and B are indicated.Study Notes – Internal Medicine James Lamberg 28Jul2010 -------------------------------------------------------------------------------------------------------------------------------------------Top 100 Secrets – Medical Secrets (4th. since it is the most sensitive measure of thyroid function in the majority of patients. early targeted and specific drug therapy. 6) Metabolic syndrome is diagnosed on the basis of abdominal obesity. 17) In patients with Coccidioides immitis infections. 2) Acute pulmonary embolism (PE) is a difficult diagnosis to establish despite newer advances in imaging. effective antimicrobial therapy. CAD-equivalent diseases. in addition to routine adult immunizations. low HDL cholesterol levels. IV catheters should be removed and ophthalmologic examinations performed to evaluate for the presence of retinal disease. age (from 40 to 79 years). keep in mind the prudent use of key diagnostic tests: (1) rapid d-dimer by ELISA is an effective screening test. 7) Pituitary tumors cause problems for patients by two main mechanisms: mass effect.
resulting in the disintegration of phytobezoars. chronic end-organ damage. look at the hand veins. but correction of iron deficiency and iron supplementation by oral or intravenous route is simpler. head and neck. more common in women who have gallstones. there is a high chance of superior vena cava obstruction. or esophagus). and hyposplenism. fragmentation hemolysis. periodic vaso-occlusive disease ("crises"). 24) Three liters of Coca-Cola administered via nasogastric lavage over a 12-hour period can dissolve gastric bezoars. 32) If a patient with lung cancer presents with hoarseness. Because up to 50% of patients develop gallbladder carcinoma. the presence of concomitant retinal disease suggests strongly (90% correlation) that the renal manifestations are due to diabetes. 29) The three major openings in the diaphragm through which hernias may occur are the esophageal hiatus (most common). especially if they continue to smoke and drink. cervix. 33) Patients with head and neck cancer have a 30% chance of developing another cancer somewhere in the aerodigestive tract (head and neck. but the problem is less frequent and smaller in magnitude with ARBs because of their less pronounced effects on aldosterone levels. 40) New onset of nephrotic proteinuria in an elderly patient warrants exclusion of an underlying malignancy. GI bleeding stops spontaneously in about 80% of patients. anus). and often by itself effective therapy. and foramen of Morgagni (rare). 36) The presence of bilateral small kidneys in a patient with azotemia confirms chronic renal failure. 25) Regardless of what is done. 42) D-lactic acidosis is characterized by increased serum anion gap. 26) Patients with hereditary nonpolyposis colorectal cancer syndrome have a higher-than-average risk of developing colon and gastric cancer. the minimum amount of free air that can be detected on an upright chest x-ray is 12mL. 38) Treatment of anemia of chronic renal failure by recombinant human erythropoietin is highly effective.Study Notes – Internal Medicine James Lamberg 28Jul2010 23) Porcelain gallbladder is an incidental finding. cheaper. and calcium oxalate crystals in the urine. 49) The triad of thrombocytopenia. 43) Ethylne glycol (antifreeze) toxicity is characterized by high anion gap metabolic acidosis. 41) The principal mechanism of bicarbonate reabsorption in the proximal tubule is through Na+-H+ exchanger (NHE3) activity. in which portions of the long arms of chromosomes 9 and 22 are exchanged. 28) In patients with suspected perforation. usually left-sided). 31) In high-risk patients. prophylactic cholecystectomy is recommended. DO NOT DISTRIBUTE -5- . 44) Bartter's syndrome is a disorder associated with normotensive hyperaldosteronism. consider and rule out renovascular hypertension. seizures. 34) If a patient presents with hypercalcemia. look for a squamous cell cancer (lung. perhaps the most spectacular of the fragmentation syndromes. It is thought that the cola acidifies the gastric contents and liberates carbon dioxide in the stomach. secondary to juxtaglomerular hyperplasia. In iron-deficiency anemia. Some patients with acute lymphoblastic leukemia (ALL) also have 9:22 translocations (poor prognostic marker). look for vocal cord paralysis. lung. and episodic encephalopathy in patients with short bowel syndrome. the TIBC is often increased. 47) Both iron-deficiency anemia and anemia of chronic disease have a low transferrin saturation. whereas anemia of chronic disease is marked by an unusually low TIBC. 27) About 90% of patients with primary sclerosing cholangitis have underlying ulcerative colitis. perform a biopsy. and fluctuating neurologic signs suggests thrombotic thrombocytopenic purpura (TTP). 50) The cytogenetic marker of chronic myelogenous leukemia is the 9:22 translocation. and severe renal potassium wasting. hypokalemic metabolic alkalosis. If the patient has a clinically suspicious lump. resulting in a shortened 22 or Philadelphia chromosome (Ph1). If the veins in the hands are distended and do not collapse when the arms are lifted over the head. 48) The main clinical manifestations of sickle hemoglobinopathies are hemolytic anemia. 37) In a diabetic patient with proteinuria. neurotoxicity in the form of ataxia. esophagus. metabolic acidosis. 45) Hyperkalemia is an important side effect of both ACE inhibitors and ARBs. a sign of mediastinal involvement (recurrent laryngeal nerve) that renders the patient inoperable. 46) Hypochromic microcytic anemias are the most encountered anemias in hospitalized and ambulatory patients. 30) In a patient who has a malignancy involving the right hilum. 39) In resistant hypertension. foramen of Bochdalex (3-5%. the chance of developing breast cancer can be reduced by about 50% with the use of tamoxifen. especially in younger (< 20 yr) or older (> 70 yr) patients. but less than 10% of all patients with ulcerative colitis have primary sclerosing cholangitis. 35) Up to 15% of breast cancers may not be detectable by mammogram.
75) There is a critical interaction between HIV and tuberculosis. 57) Incidence of lung cancer now exceeds breast cancer in women. urticaria or angioedema.. not the stroke itself. lupus. an easy way to calculate the A-a difference is as follows: (150-40/0. a large cell with two nuclei. bronchospasm. 68) ACE inhibitors are often-forgotten causes of angioedema and chronic cough. 63) A patient with low positive rheumatoid factor (RF) and arthralgia should be checked for hepatitis C. 65) Packed red cells in freshly acquired blood may include lymphocytes that can mount a graft-versus-host reaction if the patient's own immune system is unable to rapidly kill and inactivate these transfused allogeneic leukocytes. 52) Secondary monoclonal gammopathy must be distinguished from the monoclonal gammopathy associated with multiple myeloma. heart block). each possessing a distinct nucleolus. 76) If you have diagnosed one sexually transmitted disease (STD). or intrauterine growth delay. 70) Beta blockers should be avoided whenever possible in patients with asthma because they may accentuate the severity of anaphylaxis. and greatly decrease the effectiveness of epinephrine and albuterol in reversing the life-threatening manifestations of anaphylaxis. 82) Coma is usually caused by medical problems. hoarseness. 55) Assuming that you are at sea level and breathing room air. 59) Mesothelioma.8) . thrombocytopenia. 77) Most back pain is not caused by a radiculopathy. solitary plasmacytoma. 72) If you are thinking of mononucleosis as a diagnosis. premature labor. 53) Deep venous thrombosis in a young person. or malignancy. 73) Adherence to anti-HIV therapy must be > 95% for a durable response. especially HIV. It is entirely preventable. Most pulmonary disorders are associated with some degree of V/Q mismatching. HIV treatment guidelines change frequently . reflecting the distribution of these receptors in the skin. amyloidosis. 81) The sudden onset of a severe headache may indicate an intracranial hemorrhage. 67) The clinical manifestations of anaphylaxis include flushing. 66) Intranasal steroids are the single most effective drug for treatment of allergic rhinitis. TB. 79) The leading causes of death after a stroke are medical complications. benign monoclonal gammopathy of uncertain significance. 69) Chronic urticaria may require treatment with a combination of both H1 and H2 antihistamines. sense of foreboding. 78) The most common cause of dizziness is benign paroxysmal positional vertigo. 80) Heparin has no value in the acute treatment of strokes. 61) Antinuclear antibody (ANA) titers are not associated with activity of disease. nausea. This is the most common cause of hypoxemia and is responsive to oxygen therapy.always verify your information. not neurologic ones. 54) Any condition that leads to V/Q mismatching can cause hypoxemia. thrombosis at unusual sites (such as the mesenteric vein). 83) Elective surgery should be postponed for further evaluation if the patient has signs or symptoms of unstable or inadequately treated chronic disease. 60) Early. tachycardia. look for the other. Women develop lung cancer at an earlier age and after fewer years of smoking. 56) Although the anterior segment of the upper lobes may be affected by TB. 74) A person under care for HIV should not develop pneumocyotic pneumonia (PCP). malignancy). Work-up for an allergic etiology is rarely informative. lymphoma. is not associated with tobacco use.PaO2 measured by ABG. Decongestion with topical adrenergic agents may be needed initially to allow corticosteroids access to the deeper nasal mucosa. a pleural malignancy associated with asbestosis exposure. and phospholipid antibodies can significantly increase the risk for miscarriage. stridor. aggressive intervention with disease-modifying antirheumatic drugs reduces the morbidity (deformity leading to reduced functionality and disability) and mortality associated with rheumatoid arthritis. hypotension. a lesion found only in the anterior segment suggests a diagnosis other than TB (e. 58) Pleural fluid glucose < 30 mg/dL and pH < 7. or recurrent thrombosis without precipitating factors suggests a hypercoagulable state. a family history of thrombosis. pruritus. 62) COX2 NSAIDs are no more efficacious than older standard NSAIDs but are significantly less toxic. think about and test for HIV.Study Notes – Internal Medicine James Lamberg 28Jul2010 51) The classic cell seen in the lymph nodes of patients with Hodgkin's disease is the Reed-Sternberg (RS) cell. DO NOT DISTRIBUTE -6- . abdominal pain. If one infection is present. diarrhea. vomiting. and Waldenström's macroglobulinemia. headache. which can produce a low-grade synovitis and cryoglobulins (which in turn can produce a falsely positive RF). prolong its cardiovascular and pulmonary manifestations.30 suggest rheumatoid effusion. 64) Always check for Sjögren's antibodies (SSA/SSB) and phospholipid antibodies in a young woman with lupus before conception. Sjögren's antibodies increase the risk of neonatal lupus (rash.g. 71) HIV infection is preventable and treatable but never curable. and syncope. you must consider others.
not x-ray. Consider therapy before diagnostics in management DO NOT DISTRIBUTE -7- ." and encourage lifestyle changes to prevent progression to hypertension. hip pads. If the compression is caught early enough when the patient is able to ambulate. 86) All patients who take oral agents for diabetes may continue them until the day of surgery unless they have chronic liver or renal disease or are on a first-generation sulfonylurea. bilateral lower extremity weakness. and treated as any medical emergency. His past medical history is significant for prostate cancer diagnosed three years ago. 91) Always examine the feet and pedal pulses of diabetic patients regularly. instrumental activities of daily living. exercise prescription. or lithotripsy. sexual dysfunction in males. He describes the pain as band-like around the abdomen without radiation. when indicated. 95) Older adults currently constitute the fastest-growing population in the United States . So just the history of cancer with back pain means we should be evaluating this acutely. urinary incontinence. 97) Dementia and short-term memory loss are not caused by aging. assess for fall risk. given the significant mortality and morbidity of hip fractures. 94) Assess a woman's risk of coronary disease. not MRI of the spine. Jacob Levy. 88) Surgery patients on any antiplatelet agent should be told when to stop the medication before surgery and when to resume it afterward to minimize perioperative bleeding. -------------------------------------------------------------------------------------------------------------------------------------------Kaplan Videos (2001) – Neurology with Dr. injury. * The prostate cancer is important because metastatic disease to the spine could be compressing the spinal cord. and assessment of stability and mobility (e. increased tone. 93) Reduce the risk of hip fracture in elderly and high-risk patients with calcium and vitamin D supplements. Although the symptoms of diastolic and systolic dysfunction may be similar. In these cases the oral agent should be held at least several days in advance of the surgery. the traditional therapy for systolic dysfunction can actually worsen ventricular filling and increase the risk of orthostasis and syncope in cases of diastolic dysfunction. If we’re suspecting spinal cord compression. Other worrisome cancers could be breast. urinary retention. Other worrisome signs with back pain would be fever. activities of daily living. not bone scan. spastic paralysis. 92) Closely monitor patients with blood pressure measurements defined as "prehypertension. 85) Acute dyspnea in a patient who has had major surgery should raise the suspicion of pulmonary embolism. meaning do we need to intervene right now or can we treat with something like analgesics and follow-up. or reduced blood flow. 96) Commonly used instruments for a comprehensive geriatric assessment include the Mini Mental State Exam.g. and then act accordingly. the Geriatric Depression Scale. multiple myeloma. we should see upper motor neuron lesion signs below the level of the compression. worked up aggressively. as distinct from systolic dysfunction. lung. 90) Influenza virus vaccination reduces hospitalization and death from influenza and its complications in elderly and high-risk patients. 99) Diastolic dysfunction.Study Notes – Internal Medicine James Lamberg 28Jul2010 84) Patients who have undergone coronary revascularization within 5 years of a proposed elective surgery and have no signs or symptoms of recurrent ischemia can usually undergo surgery without further evaluation.a trend that is expected to continue for the foreseeable future. First thing to think about is if this is an emergency or not an emergency. positive Babinski sign. MD -------------------------------------------------------------------------------------------------------------------------------------------Spinal Cord Compression * A 61yo AAM is brought to the ED complaining of back pain that started gradually three days ago. thromboembolism. stroke. 87) Pacemakers and implanted cardioverters/defibrillators should be assessed both before and after surgery. Signs would include hyperreflexia. 89) Strict bed rest is not needed for the treatment of acute lumbosacral strain. and breast cancer before prescribing estrogen/progesterone therapy in menopause. their ability to ambulate after proper treatment is about 80%. even if the patient has received prophylaxis. looking for ulcerations.. results from impaired relaxation in heart failure with preserved ejection fraction and may account for half of all cases of heart failure in people over 80. and medications to treat osteoporosis. It is essential to ask about falls. * Patients with spinal cord compression who are unable to lift up their limbs against gravity at the time of compression have a 5% or less chance of being able to ambulate after their episode of compression. lymphoma. Tinnetti or "Get Up and Go" test). * Most likely diagnosis is spinal cord compression. 98) Delirium carries tremendous mortality and morbidity rates and should be identified. 100) Fifteen percent of elderly patients who fall and fracture a hip report prior falls. fecal incontinence. radiation therapy. Next step in the management of this patient is give dexamethasone.
Broca aphasia is expressive aphasia with intact understanding. breathing. Posterior is vertebral arteries forming the basilar artery and the posterior cerebral artery (PCA). pons. So an anterior spinal artery infarct would have lost pain/temperature sense. * Important risk factors include atrial fibrillation. then do surgical decompression. Pain and temperature lost because these spinal cord tracts are centrally located (spinothalamic). with a pool of fluid developing in the spinal cord. diabetes. sensitive maybe 80% of the time. * Risk factors for cerebrovascular disease are the same as coronary artery disease.Study Notes – Internal Medicine James Lamberg 28Jul2010 when the patient has an emergency. then do radiation. Pathophysiology is lack of blood supply to section of the brain. -------------------------------------------------------------------------------------------------------------------------------------------Syringomyelia. you note right upper extremity weakness with pronator drift and right facial palsy. * Anterior spinal artery feeds the sensory neurons involved in pain and temperature. now there is an abscess or hematoma compressing the spinal cord. An MRI shows osteomyelitis compressing the anterior cord. * Vitamin B12 deficiency causes subacute combined degeneration of the cord. patient would have facial droop and weak upper extremity. Wernicke aphasia is wordy. Most people are left-hemisphere dominant. General atherosclerosis risk factors include smoking. such as in a watershed infarct. Most sensitive test is an MRI. Vitamin B12 Deficiency & Anterior Spinal Artery Infarction * A 25yo man comes to the Emergency Department status post motor vehicle accident. * Best initial test for syringomyelia is an MRI. Say you gave dexamethasone and diagnosed. You perform a thorough neurological exam. dysphagia. focal cranial DO NOT DISTRIBUTE -8- . valvular disease (especially mitral stenosis). even if they’re showing you MRI. male gender. * Most likely diagnosis is syringomyelia. On neurologic exam. first initial step is give dexamethasone. she seems to understand what is being said but she cannot clearly respond. * MCA infarct also comes with aphasia. Characteristic signs of vitamin B12 deficiency are loss or proprioception and vibration with intact pain/temperature. HIV.” has to sleep comfortably at night. obesity. high cholesterol. and calls you to evaluate the patient. Broca is broken speech. It could be a bleed in a patient with hypertension. -------------------------------------------------------------------------------------------------------------------------------------------Cerebrovascular Accidents (CVA) * 56yo woman is brought to the ED by her daughter. and alcohol abuse. vibration/position intact. * Radiation therapy and surgical decompression are generally left for after the diagnosis is made. Aphasia occurs with dominant hemisphere stroke. circulation. Could be an embolus coming from the atrium in a patient with atrial fibrillation. Brainstem (medulla/pons/midbrain) is where cranial nerves are. Anterior is the middle cerebral artery (MCA) and anterior cerebral artery (ACA). * Focal neurologic deficit of sudden onset is very likely to be a stroke. * Basilar artery provides blood supply to cerebellum. increased age. Her daughter became concerned when her mother was unable to talk in response to her questions. ACA ischemia may involve urinary incontinence and personality changes (Phineas Gage). (CN) cranial nerves intact. Say it is lymphoma or cancer compressing the spinal cord. Most accurate test is MRI of the spine. * There is an anterior circulation and a posterior circulation to the brain. there should be an anatomic solution. So. When you question the patient. and the presence of intact proprioception/vibration sense. Best initial test is x-ray. or carotid artery disease. blurry vision. * Homunculus. Best test is MRI. (sensory) pain/temperature lost on lower extremities. Mnemonic is “put your best foot forward” for foot/leg affected with forward/anterior artery. * Patient presents with signs of cord compression. So. patient could have sudden onset of diplopia. while vibration/position and light touch are in posterior column. hypertension. unable to understand. “little man on your brain. where the clot forms in the brain itself (not an embolus from a distant site). Best initial test is a spinal x-ray. Anterior circulation on interior (leg) and middle circulation on outside (arm/face). complaining of sudden onset of right upper extremity weakness that started while she was watching television in the morning. * Most likely diagnosis is cerebrovascular accident (CVA). * Patients with MCA infarcts present with contralateral hemiparesis involving the face and the arm more extensively than the lower extremity. recent transient ischemic attack (TIA) with similar symptoms. It could also be thrombosis. Treatment is often surgical. and brainstem. * Patients with ACA infarcts presents with contralateral hemiparesis involving the leg more than the face/arm. usually with ataxia and pyramidal signs like hyperreflexia and positive Babinski. Hypotension can also induce ischemia. So he puts is feet up and lays back. nonsensical speech. The ED physician has addressed the airway. If there is an anatomic problem in the spinal cord. sudden onset of flaccid paresis. peripheral vascular disease. finding (motor) lower extremity weakness 4/5 bilaterally with some hyperreflexia. and light touch intact.
* A cranial nerve III deficit (cannot adduct eye) on one side and hemiparesis on the other is Weber syndrome. If the patient’s symptoms were due to the carotid artery stenosis. not transesophageal echo.g. * A sensory loss on one side of the face with contralateral sensory loss on the body is Wallenberg syndrome. meaning the patient is on aspirin after an ischemic stroke then has another ischemic stroke. * 56yo woman is brought to the ED by her daughter. Differentiate seizure from syncope. atrial fibrillation (24h Holter monitor). For every stroke you prevent. If there is no bleeding on the non-contrast CT.Study Notes – Internal Medicine James Lamberg 28Jul2010 nerve palsies. the stenosis would be on the left side (not the right). PCA ischemia comes with hallucinations. because these two have different management. * Hemorrhagic stroke is managed by supportive care and consulting neurosurgery (poor prognosis). you’re looking for the presence of white material in the parenchyma of the brain. PT > 15sec. * Say you do a workup on the 56yo lady that has right-sided facial/arm hemiparesis. * Ticlopidine is never the answer due to side effect. GI bleed. * With posterior circulation (basilar artery). The difference between clopidogrel and ticlopidine is that ticlopidine causes the side effects (TTP. say due to arrhythmia. * Contraindications for tPA therapy are bleeding (e. -------------------------------------------------------------------------------------------------------------------------------------------Seizures * 29yo man is brought to the ED by ambulance after his mother found him convulsing in his bedroom. tPA. * Must document time of onset and CT scan with diagnosis before giving tPA. giving us the ability to see. ischemic stroke or head trauma within 3 months. or stroke in evolution. add dipyridamole. * Heparin reduces the rate of recurrent CVA. the tissue will look darker than the surrounding tissue. carotid artery stenosis (carotid artery duplex. not aspirin. not transthoracic echo. The benefit of aspirin in acute stroke is not as good as with acute myocardial infarction. or is allergic to clopidogrel. Carotid duplex finds 80% stenosis of the right internal carotid artery. CT shows no bleeding. tPA should not be given even if you get the CT minutes later. mainly for anterior circulation stroke). a loss of brain function occurs with brain cell death. then answer is tPA/PLAT (tissue plasminogen activator). * Aspirin is used in ischemic stroke for secondary prevention. not tPA. * When looking at a CT scan to evaluate a suspected CVA. Symptoms mean you have to be able to blame a TIA or a stroke on the stenosis. Her daughter became concerned when her mother was unable to talk in response to her questions. failed aspirin therapy. we assume ischemic stroke. surgery within past 14 days. CT scan without IV contrast is most sensitive test for hemorrhagic stroke.g. * With ischemic stroke. * Clopidogrel is used if the patient has failed aspirin therapy. and a motor deficit (hemiparesis. A cross syndrome is a cranial nerve deficit on one side.000. MRI most sensitive for posterior fossa lesions. So the risk to benefit ratio is not favorable after 3 hours. and symptom onset is within 3 hours. but we give it anyway. not heparin. she seems to understand what is being said but she cannot clearly respond. you are sure it is ischemic stroke. basilar artery thrombosis. In ischemic stroke. you note right upper extremity weakness with pronator drift and right facial palsy. The mother says he was tired and lethargic for 20 minutes after the episode. complaining of sudden onset of right upper extremity weakness that started while she was watching television in the morning. not clopidogrel. She then called the ambulance to bring her son to the hospital. not ticlopidine. * Most sensitive (accurate) test for diagnosing ischemic stroke is MRI. * If the patient is allergic to aspirin. Now. For ischemic stroke. which are TTP and neutropenia. * What is the most likely diagnosis? Answer is seizure. BP > 185/110. intracranial bleed ever in the past. * If patient was sleeping and woke up with symptoms. urinary tract bleed) within past 21 days. ataxia) on the opposite side. Answer is head CT without contrast. DO NOT DISTRIBUTE -9- . So the only time you give heparin is when you have a higher risk of CVA. you cause one complication (e. ticlopidine. If you give tPA past the 3-hour window. Most likely diagnosis is MCA infarct (left side). Cerebellar signs include ataxia and vertigo. you’re only increasing their risk of bleeding. On neurologic exam. neutropenia) more often. visual loss. Answer is not surgery. The patient’s mother said that her son was unable to respond to her frantic cries during the convulsion and describes jerking motions that become more frequent then stopped after about 1 minute. Indication for carotid endarterectomy (CEA) is >70% stenosis with symptoms. There is a higher risk of recurrent CVA if the patient has ischemic stroke with atrial fibrillation. heparin. * Patient has arm/face hemiparesis and Broca aphasia. Next step in management is head CT scan. Clopidogrel side effects include TTP and neutropenia. When you question the patient. look for reversible risk factors such as cardiac thrombosis (echocardiogram). we can think about giving aspirin. * PCA supplies occipital lobe. deficit is contralateral if above decussation and ipsilateral if below. do we give contrast or no contrast? We are trying to distinguish between a bleed and ischemia. clopidogrel. * Stoke in evolution is when symptoms are getting worse. * If patient has acute onset focal neurologic deficit. We are looking for the absence of blood. Cross syndrome is most likely posterior circulation stroke. platelet count < 100. * A cranial nerve III deficit on one side and ataxia on the other is Benedikt syndrome. bleed).
So patient might have shaking/jerking of the hand. If you identify a secondary cause. Urinary or bower incontinence is an important part of the history. metabolic (electrolytes. * What if patient continues to seize after giving phenytoin or fosphenytoin? Give phenobarbital. when do you start treating an idiopathic seizure? Answer is with recurrent seizures. * Medication for absence seizure is ethosuximide. An atonic seizure means lack of tone. think about metastatic to the brain. drugs). Then what do you give? Answer is phenytoin or fosphenytoin. low oxygen. meningitis). * Seizure Meds: ABC. low calcium. so patient keeps postural tone but brain shuts down so the patient is not paying attention (no consciousness) and likely just blinking. * Say you give the benzo and the patient is still seizing. What is the best initial treatment now? Answer is give lorazepam or diazepam. Bite marks on the tongue may imply seizure. Ask if the patient has a history of epilepsy. hoping seizures resolve. the post-ictal state still is the most specific symptom. and the patient is already intubated. low glucose. We follow the patient. So this is the clear differentiation. low-grade fever with weight loss. primary tumors). order an EEG. A complex partial seizure is treated differently from a complex generalized seizure. or photophobia. * Medication for atonic or myoclonic seizure is valproic acid. * A partial seizure only affects one part of the brain. look for risk factors and sudden onset of neurologic focality. A simple seizure has no loss of consciousness. Syncope has rapid recovery within minutes or seconds after unconsciousness. A generalized seizure affects the entire cortex. Note. give fosphenytoin instead.10 - . * Seizures are categorized into partial. phenobarbital. purpura. * A seizure is defined as random firing of neurons in the brain.Study Notes – Internal Medicine James Lamberg 28Jul2010 This patient was having convulsions (tonic-clonic movements). arthritis. Either the seizure starts as generalized. SLE). and last midazolam/propofol. So patient has first time seizure with no exact etiology. A complex seizure implies loss of consciousness. * Ask yourself if there is an underlying cause for the seizure. or the foot. Patients who have syncope and come out will not be lethargic. A seizure is considered a complaint. If a young woman with breast cancer has a seizure. giving phenytoin IV is not recommended due to lack of solubility and resultant precipitation. or with achy muscles. and complex vs. breathing. If patient came in hypoxemic and seizing. treatment would be focused on hypertonic saline. If the patient has positive family history. * Seizure: vascular (stroke. * If you’re thinking vascular disease. Do not assume that any seizing patient has a diagnosis of epilepsy. The most specific thing on history for seizure is the post-ictal state. high sodium. * So patient has normal neurologic exam. * Urinary and bowel incontinence plus bite marks are seen more commonly in seizure than syncope. and circulation. Management is lorazepam or diazepam. or nuchal rigidity. Myoclonic seizures involve muscle jerks. but not specific either. idiopathic. positive ANA. there is a large differential diagnosis for seizure. but not necessarily specific. treat it. Categories help determine what medication to give. * Medication for unidentifiable seizure is valproic acid. look at things like low sodium. so patient has “drop attacks. Blood pressure and circulation are intact. * Next step after phenobarbital? Answer is midazolam and propofol (anesthesia). SLE stigmata. For metabolic. or the leg. glucose. like a patient coming in with chest pain. * 29yo man comes in with new-onset seizure witnessed by his mother. * Medication for partial seizure (even one that becomes generalized) is carbamazepine or phenytoin. low magnesium. lorazepam/diazepam. pick valproic acid. simple. If carbamazepine or phenytoin are not answers. So if patient comes in seizing with sodium of 106. DO NOT DISTRIBUTE . Patient is continuing to seize. the patient was tired/achy for 20minutes. we start treatment. phenytoin/fosphenytoin. negative family history. bleed. generalized.” An absence seizure is the opposite of an atonic seizure. * What is the best test to identify abnormal neural activity that predisposes to a seizure? Answer is electroencephalogram (EEG). neoplastic (metastatic cancer. * The next step in management is ABCs: airway. Then benzodiazepine. convulsing with a long post-ictal state. tired. negative EEG. * Always look for a secondary cause. However. * What if EEG is negative. or a partial seizure turns into a generalized seizure. we would start right away at the first seizure. * If patient is continuing to seize without regaining consciousness between. and one seizure. infection (encephalitis. AVM). autoimmune (vasculitis. treatment would be focused on intubation and high-flow oxygen (after ABCs). * Seizure differential mnemonic: VITAMINS. Suspect autoimmune if history involves a rash. Suspect infection if the patient has seizure with fever. s for Psi or psychiatric (patient faking). Patients who syncopize can have tonic/clonic movements. this is status epilepticus. Here. trauma. as it is the most widely effective seizure medication. Once the patient has another seizure. for acutely seizing patient. * Medication for generalized seizure is valproic acid or lamotrigine.
Physical exam finds a resting tremor noted in his right hand. the answer is selegiline. * Acetylcholine blocking with trihexyphenidyl primarily. more so than younger patients. history of falls (postural instability). Exam for cerebellar disease would include finger-to-nose and heel-to-shin tests. diagnosis of Parkinsonism is clinical. and cerebellar disease. She also states that her husband has been moving very slowly as of late. and ropinirole. In cerebellar disease. You can decrease the amount of dopamine by antagonizing it (decreasing it directly) or by increasing acetylcholine. the patient will have pillrolling tremor at rest. When questioned. Pick trihexyphenidyl if patient is < 60yo. * Dopamine agonists are bromocriptine.g. the tremor occurs primarily with movement (intention tremor). We don’t give carbidopa/levodopa to functional patients because it has the most serious side effects. Is this patient diabetic and taking metoclopramide for autonomic neuropathy with gastric paresis? * Most cases of Parkinson disease are idiopathic. His past medical history is significant for mild hypertension treated with a thiazide diuretic. and when walking the patient is stooped forward making small steps. patient turns in wide circle. With postural instability. pramipexole. bleed or stroke. Know that patients will present with abnormal movement (chorea). * Say patient is functional and just has a tremor. and there are no other stigmata of cerebellar or Parkinson disease. and amantadine increase dopamine amount/effect also. Carbidopa inhibits the conversion of levodopa to dopamine in the periphery. MPTP: an unintentional byproduct of the recreational drug MPPP). how do they function on a day-by-day basis? * Functional patients get amantadine or anticholinergic (e. carbidopa/levodopa. the patient experienced uncontrolled grimacing with grunting. trihexyphenidyl). So. like ropinirole (not selegiline or COMT inhibitor). In Parkinson disease. slow movement (bradykinesia.Study Notes – Internal Medicine James Lamberg 28Jul2010 -------------------------------------------------------------------------------------------------------------------------------------------Parkinson Disease * A 56yo man is brought in by his wife for evaluation of a resting tremor that she noticed recently. * Say patient has stigmata of Parkinson and you are asked what medication is thought to arrest the progression of Parkinson disease. We avoid anticholinergic medications in elderly patients because they can become confused. so that the levodopa can reach the brain and be converted to dopamine there. So ask yourself about secondary causes. Response fluctuations are the “on/off phenomenon. tumor. * Side effects are psychosis. add the dopamine agonist. meaning we cannot identify a cause. manganese. ropinirole) to treat response fluctuations for patients that are taking carbidopa/levodopa. with the patient have a compromised ability to reach the object. On/off phenomenon is quite distressing to patients. * Always ask how much function you are getting from the treatment at the expense of the side effects. * Normally when you walk and turn it is a smooth movement. paucity of movement). pramipexole. or to take away acetylcholine so the dopamine in the brain can work more effectively. essential tremor. and cogwheel rigidity (arm feels like cogs on a wheel. * The drugs that cause Parkinson are antipsychotics. * So in the 56yo man with resting tremor. * Most likely diagnosis is Huntington disease. * The most preferred dopamine agonists are the newer ones. and acute GI upset. dry mouth. the tremor occurs at rest and resolves with movement. patients get response fluctuations. You can also give a COMT inhibitor or selegiline. Recently while sitting at a family dinner. the most effective treatment for Parkinson disease.11 - . metoclopramide. COMT inhibitors. dry eyes. * Causes of Parkinsonism are drugs (antipsychotics. and dyskinesia (abnormal movements). * Differential diagnosis for tremor includes Parkinson disease.g. cobalt. DO NOT DISTRIBUTE . pick amantadine if patient is > 65yo. * Parkinsonism is defined as death of dopaminergic cells in the substantia nigra.” akinesia (restlessness). what is the most likely diagnosis? Answer is Parkinson disease. * Non-functional patients get carbidopa/levodopa. thus we can give less levodopa and get the same effect. moving in distinct steps). His family history is significant for his father who died at age 41 of dementia. -------------------------------------------------------------------------------------------------------------------------------------------Huntington Disease * 34yo man comes to your clinic for evaluation of strange spontaneous movements that have been occurring lately. the tremor occurs and worsens with movement. pergolide. In essential tremor. In Parkinson disease. there is a family history usually. the patient states that he feels fine and does not know why his wife is dragging him from doctor to doctor. After long-term therapy on carbidopa/levodopa. * If patient is on carbidopa/levodopa and it isn’t enough. which are dopamine antagonists. * Selegiline (MAO-B inhibitor). have urinary retention. hypotension. * So how do you choose what to answer as the best initial treatment for Parkinson disease? First question to ask your self is what is the functional status of the patient? Meaning. You note cogwheel rigidity in his right upper extremity with a positive Myerson sign (patient unable to resist blinking with glabellar tapping). * Answer dopamine agonists (e. Acetylcholine acts to inhibit dopaminergic tone in the brain. CO poisoning. So treatment is to either give dopamine to provide what is lost.
* Treatment for fatigue in MS is amantadine. Primary progressive disease has worsening MS symptoms right from presentation. frontal lobe neoplasm and chronic subdural hematoma (check for focality on exam or trauma history). and carpal tunnel syndrome. In Alzheimer disease. * Most common cause of dementia is Alzheimer disease. looking for chromosome 4p CAG repeat. * Non-reversible causes: Creutzfeldt-Jakob disease and prion disease (check for myoclonus. speak with spouse). Physical exam is unremarkable. When asked. coronary artery disease. vitamin B12 deficiency (check B12 level). and olfactory/visual evoked potentials looking for abnormal transmission. central or obstructive sleep apnea (look for obesity. and high cholesterol. but not in primary progression. waxing/waning). not lumbar puncture. * The essential point for clinically suspecting MS is a patient with multiple neurologic deficits that are separated by space (anatomically) and by time (temporally). but they help symptomatically for the disease relapse. difficult to differentiate from Alzheimer). * Differential includes MS. * Treatment for acute exacerbation of MS is IV high-dose steroids with a 4-week taper on oral prednisone. LFTs. Her past medical history is significant for hypertension. * Relapsing/remitting disease can become progressive (secondary progression). CSF for oligoclonal banding. -------------------------------------------------------------------------------------------------------------------------------------------Multiple Sclerosis (MS) * A 32yo woman comes to the ED with numbness and tingling in her right hand. No medication has been shown to help with primary progressive disease. Lewy body disease (delirium-like course. * Treatment is supportive care. violence. * Olfactory/visual evoked potentials are not used much today with the development of MRI.Study Notes – Internal Medicine James Lamberg 28Jul2010 abnormal behavior. DO NOT DISTRIBUTE . * The best initial test is also MRI. cervical spinal disease. interferon beta 1b. She states that her symptoms began several days before admission and have progressively worsened over the last several hours. uremia and cirrhosis (check creatinine. there is initial memory loss that becomes chronic and gradual with relative preservation of social function and personality until late in the disease. then get the lumbar puncture. None of these three is better than the other. * Most likely diagnosis is multiple sclerosis (MS). * Treatment for spasticity in MS is baclofen. tie temporally dementia onset with CVA. * Clinical diagnosis is presence of chorea with personality changes. rapid dementia course usually weeks to months). HIV. She states that recently she has been forgetting telephone numbers and cannot remember the name of her mailman who she has known for 25 years. such as agitation. least common. 85-95% sensitive. multi-infarct dementia (stepwise progression. changes in personality. Looking for multiple lesions and paraventricular lesions consistent with MS. You also note increased spasticity in her lower extremities. there is no formal treatment. Steroids do not slow down the progression of the disease. * CVA less likely because she is 32yo with no other listed risk factors. True diagnosis done with genetic analysis. or glatiramer acetate. * Testing includes MRI with gadolinium. physical exam). * Medications useful to arrest the progression of MS are interferon beta 1a. * Brain tumor less likely as there is no specific tumor location giving lower extremity weakness along with diplopia. she states that three years ago she had an episode of seeing double that lasted two days that resolved on its own. * Treatment for urinary incontinence in MS is oxybutynin. usually in a patient 30-40yo with a positive family history. * Relapsing/remitting disease is a form of MS where patient goes through waxing/waning episodes of symptoms. They have been shown to help with relapsing/remitting forms.12 - . * Pick disease (frontal lobe degeneration) has personality changes initially. * Cervical spinal disease or carpal tunnel less likely because they do not explain the diplopia. * Reversible causes: hypothyroidism (check TSH). syphilis (check RPR: rapid plasma reagin). * What is the most sensitive/accurate test? Answer is MRI or brain and spine. consider dementia and ask yourself if there is a reversible cause. -------------------------------------------------------------------------------------------------------------------------------------------Dementia * A 67yo woman is brought to your clinic complaining of forgetfulness. * With memory loss. Physical exam is significant for hyperreactive reflexes bilaterally in the lower extremities. and a family history of a similar thing happening to a first-degree relative (Huntington is autosomal dominant). * Treatment for urinary retention in MS is bethanecol. and worse prognosis. CVA. loss of inhibition. not CT scan. brain tumor. * If MRI is inconclusive or equivocal for the clinically suspected MS diagnosis.
we do MRI. Treatment is meclizine (antihistamine) or diazepam in severe cases. Patient may say the room is spinning around me. such as concentration. * Labyrinthitis is peripheral vertigo that occurs when vertigo follows an upper respiratory tract infection. * Migraines are associated with triggers. hearing loss. CJD (myoclonus. what is the likelihood that this headache is secondary to some serious underlying pathology? Is this a brain tumor? Meningitis? Subarachnoid bleed? Do we need to diagnose and intervene immediately? * History/physical implying serious underlying cause: first time headache with severe pain. chocolate). For central. * Medication of choice for Alzheimer now is donepezil. for peripheral. The patient describes walking to her bathroom and experiencing a sudden feeling of nausea. light headed. Most likely diagnosis is a migraine. MS. * Ask yourself. or executive function. sleeping too little. * Patient presents with memory loss. This implies cardiac disease. thunderclap headache (time to peak pain was seconds). Etiology is thought to be an otolith in the semicircular canals. like they are falling forward. She admits to nausea but denies vomiting. low salt diet. This is where the mini-mental status exam (MMSE) is important. usually vertical). She describes the feeling of the room spinning around her even though she realizes she is not moving. * Benign positional paroxysmal vertigo (BPPV) is peripheral vertigo of sudden onset related to movement of the head. palpitations. if you find central vertigo signs on physical exam.g. posterior fossa tumor. “worst headache of my life” (subarachnoid).Study Notes – Internal Medicine James Lamberg 28Jul2010 * Dementia is generally memory loss plus some other deficit in cognitive function. neighborhood signs (cranial nerve deficits via brainstem). She managed to reach the bathroom where she vomited once and fell to the floor a second time. Does the patient mean they are having vertigo or do they mean pre-syncope? * Pre-syncope associated symptoms are feeling like going to black out. any headache starting at age > 55yo. and tinnitus unrelated to head movement. * Differentiating between vertigo and pre-syncope is a clinical determination. nystagmus suppresses with fixation. fever. but no longer used as the drug of choice due to liver toxicity. nuchal rigidity. -------------------------------------------------------------------------------------------------------------------------------------------Headache * A 32yo woman comes into the office complaining of a headache that started two days ago. DO NOT DISTRIBUTE . * Primary headache disorders include migraine. Perform MMSE to find dementia. On exam. * Next question after determining vertigo is if it is central (in the CNS. Treatment of choice is diuretics. * Most important question is to identify what the patient means by dizziness. Then rule out non-reversible causes like Pick (personality changes first). rapid progression). mixed nystagmus (usually horizontal but with another component). worse in the early morning. “Dizzy” is very nonspecific and does not have much significance medically. cluster. the earth is rolling in front of my feet. such as eating a specific food (e. and surgical decompression if medical management fails. * So. nystagmus non-suppressible with fixation. BPPV. symptoms aggravated by cough. shortness of breath. and tension. pure nystagmus (in one direction. chest pain. seek Meniere. focality on CNS exam. -------------------------------------------------------------------------------------------------------------------------------------------Vertigo * A 53yo woman is brought to the ED complaining of dizziness. uni-directional nystagmus * Posterior fossa imaged more effectively with MRI than with CT scan. Treatment of choice is movement exercises to try and move the otolith out of the canal. Physical exam can reproduce symptoms via Dix-Hallpike test (head movement testing). headache occurs after vomiting. * Central vertigo is usually chronic. or labyrinthitis with their treatments listed. Now. we diagnose Alzheimer disease. She locates her headache to the right side of her head and describes it as pulsating and throbbing in quality. * Vertigo is the sensation of movement in the absence of movement.g. tinnitus. She was unable to get up off the floor and called 911. give meclizine initially then diazepam secondary. She also states that loud noise and bright light exacerbate her pain. aggravated by valsalva maneuver. we do symptomatic treatment. * Treatment for Alzheimer disease was tacrine. she has had these headaches a few times before. Do not pick tacrine for first line. there is no focality on physical exam. Disease is thought to be caused by swelling in the semicircular canals. If you identify peripheral vertigo. and Lewy body (delirium-like). stress. praxis. The headache is worsened by walking up stairs or around the block. A trigger is very specific for migraine. * Ménière disease is a triad of (peripheral) vertigo. e. Then rule out or treat reversible causes. Patient may say I move my head then 5-10 seconds later I get dizzy. do MRI imaging of the posterior fossa. or during menstruation. progressively worsening headache. hearing loss. multi-directional nystagmus * Peripheral vertigo is usually acute. * If you cannot identify a disease. medication) or peripheral (ear semicircular cannals). multiinfarct dementia (temporal tie to CVA).13 - .
or verapamil. there typically is not a distal to proximal movement. prednisone. Migraines are generally caused by vasodilation and sumatriptan constricts the vessels. or methysergide (generally not used because it causes retroperitoneal fibrosis). She notices that her symptoms improve following a good night sleep. radiating to neck or back of the head. * Management for cluster headaches starts with 100% oxygen. vice-like. Do not give it even if you have high suspicion of CAD. * Cluster headaches are usually unilateral (like migraine). possibly Horner syndrome (ptosis. seen in HIV. So you’re looking for high protein and few cells. DO NOT DISTRIBUTE . ptosis. In the context of clinical suspicion of myasthenia. myasthenia gravis (MG).Study Notes – Internal Medicine James Lamberg 28Jul2010 * Pulsatile headaches occur in cluster and migraine headaches (both vascular). looking at CSF for high protein that is not accompanied by pleocytosis (a high number of cells). no trigger. The patient states that his symptoms began two days ago. miosis. CIDP (chronic) has a slower course. so IV Ig best initial treatment. anti-acetylcholine receptor antibody is extremely specific for the diagnosis. an AIDP. like acetaminophen or NSAIDs. distribution starts in distal areas and moves proximal. the patient is noted to have bilaterally lower extremity weakness with loss of reflexes. On neurologic exam you notice snarling appearance when the patient is asked to smile and a nasal tone to her speech. red eye. Prophylaxis for cluster headaches includes lithium. * The best initial test for the diagnosis of GBS is lumbar puncture. Patients complain of easy fatigability. A tensilon test is not the initial test. * Management for mild migraine headache (no nausea or vomiting). * A positive tensilon test is not specific for the diagnosis. Lou Gehrig disease). give NSAIDs. Approximately three weeks ago the patient states that he experienced several episodes of diarrhea that resolved spontaneously. In Guillain-Barré. The patient also complains of difficulty chewing meat and other hard foods. Prophylaxis for migraines is indicated when patient has more than 3 headaches per month. * Only answer tensilon testing when there is no answer choice for acetylcholine receptor antibody. * In MG. * The distribution of weakness is important when differentiating between Guillain-Barré. sweating) are also seen. Do not give prednisone or systemic steroids in the treatment of acute Guillain-Barré syndrome. abortive therapy is sumatriptan or ergot alkaloid. occurring in clusters. IVIG and plasmapheresis are equivalent in their effect. and botulism. are bilateral. * Management for tension headache is analgesics. -------------------------------------------------------------------------------------------------------------------------------------------Acute Inflammatory Demyelinating Polyradiculoneuropathy (AIDP) * A 46yo man is brought to your office complaining of rubbery legs. You also note weakness of the upper extremities when the patient is asked to clench her fists around your fingers repeatedly. * Hyporeflexia seen in any peripheral neuropathy. you just gave them an MI. So if a patient has a 70% left main coronary lesion and you give them sumatriptan. * The best test (most accurate) for GBS is an electromyogram (EMG). You can also do plasmapheresis. * Tension headaches are triggered by stress but not foods or emotion. anhidrosis). false positives seen in other diseases like amyotrophic lateral sclerosis (ALS. diplopia). timolol. * Best initial treatment for GBS is intravenous immunoglobulin. * Photophobia and phonophobia (ligyrophobia) classically occurs in migraine but may occur in cluster also. Cluster headaches peak usually within 5 minutes (quick onset) and only last 45-90 minutes. * Migraines peak within 4-72 hours from onset of pain (gradual onset). On neurological exam. Paresthesias (tingling) and autonomic instability (labile blood pressure. If migraine is moderate to severe. Symptoms are not acute either.14 - . Next line is sumatriptan. -------------------------------------------------------------------------------------------------------------------------------------------Myasthenia Gravis (MG) * A 35yo woman comes to the clinic complaining of double vision that seems worse near the end of the day. * Clusters happen 2-3 times per day over a 4-8 week period. Prophylaxis is propranolol. IV Ig is easier to give than arranging for plasmapheresis. * Never give sumatriptan to a patient with a history of coronary artery disease. * Most likely diagnosis is myasthenia gravis (MG). * MG is defined as muscle fatigue after repetitive motion of chronic onset with preferential involvement of the ocular and the pharyngeal muscles. * Campylobacter jejuni infection (gastroenteritis) associated with Guillain-Barré syndrome (GBS). especially in the muscles of the throat and eyes (dysphagia. * The best initial test for diagnosing myasthenia is serology for the anti-acetylcholine receptor antibody. has rhinorrhea. * Most likely diagnosis is Guillain-Barré syndrome.
Study Notes – Internal Medicine
* The best (most accurate, most sensitive) test for the diagnosis is electromyography (EEG) looking for a decrease in the action potential spike on repetitive stimulation. * MG is essentially an autoimmune disease against the acetylcholine receptor. * Treatment is symptomatic for weakness and for the disease with autoimmune suppression. * Symptomatic treatment is with anticholinesterase medication (neostigmine, pyridostigmine) to raise the level of acetylcholine in the synapse, improving the weakness. * To treat the autoimmune disease, give prednisone, azathioprine, IV immunoglobulin, plasmapheresis, and thymectomy. Prednisone is best initial immunosuppressive because it takes 1-3 months to have an effect. Patients may initially have a worsening of their disease. Azathioprine takes 3-6 months to have an effect. * If acute myasthenic crisis, use IVIg or plasmapheresis to improve the patient’s crisis immediately and acutely. * In patients with GBS or MG, you must follow their respiratory status. The diaphragm is a skeletal muscle and when the disease involves the diaphragm the patient can go into respiratory failure. So, always consider the possibility of an intubation and respiratory support to get them through the crisis. -------------------------------------------------------------------------------------------------------------------------------------------Kaplan Videos (2001) – Pulmonology with Dr. Asher Kornbluth, MD -------------------------------------------------------------------------------------------------------------------------------------------Read the last line of the question stem to help determine what organ system the question is asking about. This will help you develop a better differential diagnosis as you read the question. -------------------------------------------------------------------------------------------------------------------------------------------Pulmonary Function Tests * A pulmonary function tests (PFT) is generally used to differentiate between obstructive and restrictive disease. There may be a great deal of overlap between these. * Tidal volume is normal in-and-out respiration at rest. Good rule of thumb is 10mL/kg, so 700mL for a 70kg patient. Vital capacity is deep breath then exhaling maximally, does not empty lungs completely. Residual volume is left over lung volume after vital capacity. Vital capacity plus residual volume is total lung capacity. Residual volume is a difficult measurement to make and not done in clinical practice, so you never know the exact total lung capacity. * In restrictive pattern, all lung volumes are decreased. Therefore total lung capacity is decreased. Lungs are restricted and cannot expand due to disease such as sarcoidosis, interstitial fibrosis, and chronic tuberculosis. * In obstructive pattern, there is an obstruction in getting air out of the lungs; a hallmark of asthma and chronic obstructive pulmonary disease (COPD). Residual volume will be higher because you cannot expel all of it. Over years, the total lung capacity will increase with increased residual volume. This is what causes the large AP diameter, giving the barrel chest appearance. Measures of air outflow are reduced in obstructive disease. * FEV1 measured by having patient take deep breath in then breath out as fast as possible, with the forced expiratory volume measured over 1 second. * FVC is the forced vital capacity, basically the same as vital capacity. * FEV1/FVC ratio is decreased in obstructive disease, mostly because FEV1 is low. So FEV1 and FEV1/FVC low. * FEV1/FVC ratio is normal in restrictive disease, with low FEV1 and low FVC. * FV25-75 is forced volume between 25% and 75% during a vital capacity. FV25-75 reduced in obstructive. * Residual volume high in obstructive lung disease, low in restrictive lung disease, but RV not easy to measure. -------------------------------------------------------------------------------------------------------------------------------------------Alveolar-Capillary Membrane Diffusion * Diffusion capacity is a measure of alveolar capillary membrane, not an easy measurement to do. Alveolarcapillary membrane gets destroyed/fibrosed in emphysema. If the DLCO (diffusion of the lung carbon monoxide) is low, implies destruction of the alveolar-capillary membrane, so emphysema or ARDS (acute respiratory distress syndrome). ARDS patients are generally in the ICU on a respiratory so a DLCO isn’t measure. * In bronchitis DLCO may be normal, in emphysema DLCO may be low. * Simpler way to measure gas exchange effectiveness is by measuring alveolar-arterial difference in oxygen, the AaDO2 or Aa gradient. This involves getting an arterial blood gas (ABG) after performing an Allen test to ensure ulnar collateral circulation (not sensitive but still done). On ABG, lab gives you pH, PCO2, PO2. * Say PO2 80mmHg (normally 90-100). Alveolar O2 at room air (21% O2) is 150 - 1.2*PCO2. * Normal PCO2 is 40, so Alveolar O2 would be 150 - 1.2*(40) = 102. Difference is achieved by subtracting what O2 you got in the blood gas (80mmHg), so 22 here. This is mildly elevated as normal is 5-15. * If there is a pulmonary process affecting the membrane, A-a gradient may be as high as 40. * Say our ABG comes back as 7.4/20/100. Alveolar is 150-1.2*20 = 126. 126-100 (PO2) gives 26 for Aa gradient. * Think about this physiologic process. The patient is breathing very fast to get PCO2 down to 20, so you know there is some problem. That is why measurement of PO2 does not tell you what kind of gas exchange you have.
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Study Notes – Internal Medicine
* So in summary, A-a gradient tells you what is going on for gas exchange at the alveolar-capillary membrane. * Given 7.4/36/96. Find Aa gradient. 150-1.2*36=107. 107-96 is 11 for Aa gradient (normal range). -------------------------------------------------------------------------------------------------------------------------------------------Solitary Pulmonary Nodule * A solitary pulmonary nodule is a single nodule less than 6cm. Lung cancer is rarely cured. The only time you can cure is if you have a solitary cancer and resect before it metastasizes. * So you found a < 6cm nodule on chest x-ray. What are the criteria for just following this nodule? Young patient (<50yo) and non-smoker. If this is the case, repeat the chest x-ray every 6 months for 2 years. If the nodule has not changed size, we know it is benign. Tell patient to take CXR with them next time they go for an x-ray. * If you are looking for calcification within a nodule, do a chest CT scan due to increased sensitivity. * Popcorn appearance (scattered areas) of calcification within nodule, think hamartoma (e.g. hair, tooth). * Central or bull’s-eye calcification within nodule, think granulomatous disease (e.g. tuberculosis). * Eccentric (near edge) single area of calcification within nodule, think possible malignancy. * Say patient is 60yo and 50pack*year smoker. You find a 2cm nodule on CXR. Next step is do a biopsy, most of the time by open lung biopsy. Usually nodule is not central enough to reach with simple bronchoscopy. If the biopsy shows malignant cells, next step is surgery to remove. If benign, follow with CXRs. -------------------------------------------------------------------------------------------------------------------------------------------Pleural Effusion * The pleura covering the organ (the viscera) is the visceral pleura. The pleura outside that is the parietal pleura, with fluid between the two pleurae. When fluid increases between these two, this is a sign of a pleural effusion. * Early sign of pleural effusion is loss of costophrenic angle at the diaphragm, requires about 300mL of fluid. * Lay patient on the side of the effusion and do a lateral decubitus x-ray. If the effusion is free-flowing, the fluid will layer out into the dependent portion. This is useful to know to determine if you will get fluid via thoracentesis. If the fluid were trapped, we have to hit the trapped portion itself. * Pleural effusions classified into transudate and exudate. In general, exudate is seen in sicker patients. Transudate is seen in high-pressure differences (e.g. CHF) or low blood oncotic pressure (e.g. nephrotic syndrome, cirrhosis). Cirrhosis causes hypoalbuminemia (protein not created) typically resulting in right pleural effusion. * To differentiate, need pleural LDH and protein, with comparison to serum LDH and protein. Transudate has low LDH (<200) and low protein. Pleural to serum LDH < 60% and pleural to serum protein < 50%. * Transudate typically caused by systemic diseases. Exudates typically caused by lung diseases. * Exudate: pleura has some process that causes it to exude fluid. The larger the effusion, the safer the thoracentesis. * Say we do the tap and the LDH is 300 and protein is 3grams (high). This is an exudate. * Exudate causes include cancer, tuberculosis, pulmonary embolus with infarction, pneumonia. If infected material exudes out (parapneumonic), we have a complicated effusion and need a chest tube to drain else it scars and the patient loses lung volume. This scaring can happen quickly. * Complicated exudative effusion (requiring chest tube) includes infection with pH < 7, pus on tap, polys on gram stain, and low glucose in fluid. Next step is chest tube, not antibiotics, not intubation, not further diagnostic studies. * Parapneumonic effusion leaks fluid but no low pH, no pus, no polys on gram stain, not low glucose. So this is an uncomplicated parapneumonic effusion. This patient does not need a chest tube. So patient has fever, pneumonia, and effusion. Next step is put a needle into the space to determine if it is complicated. If not, just treat pneumonia. * Empyema is an effusion with pus in the space, requires a chest tube. -------------------------------------------------------------------------------------------------------------------------------------------Atelectasis * A 62yo man is dyspneic 24hours after cholecystectomy. His respiratory rate is 22, and pulse is 112, has a mild fever, and decreased breath sounds are noted in the left lower lobe. CBC shows leukocytosis of 27,000. * Patient is post-op with anesthesia medication causing decreased lung expansion, is on narcotic meds and likely not taking in deep breaths because of pain. Most likely diagnosis is atelectasis. * Atelectasis is collapsed alveolar airways, lung itself is not condensed on itself. * Massive ascites pressing up on lungs and impairing ability to take deep breath can cause atelectasis. * Broken ribs causing pain on inspiration can cause atelectasis. * This can give rhonci or crackling at the bases, perhaps a little wheezing. * You can get mild fever with atelectasis. Post-op surgical “W”s of fever: Wind (atelectasis), Water (UTI), Walking (DVT), Wound (incision infection), Wonder drugs (drug causes) for days 1, 3, 5, 7, and 9. * Next step in diagnosis is chest x-ray. * Treatment is inspired spirometry breathing device, also known as incentive spirometry.
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Study Notes – Internal Medicine
-------------------------------------------------------------------------------------------------------------------------------------------Chronic Obstructive Pulmonary Disease (COPD) * Patient has COPD, is a non-smoker, liver problems, and has relatives that died of lung or liver problems. Think alpha-1 antitrypsin deficiency. Patient can have either liver or lung involved, not necessarily both. * Treatment is symptomatically, recurrent antibiotics, hoping they do not need a lung or liver transplant. * COPD patients can develop pulmonary hypertension, giving a loud second sound on heart exam (P2). During inspiration, right-sided heart pressures increase. So here the second heart sound will get louder on inspiration. Patient may have a right-ventricular heave, and ECG may show right-ventricular hypertrophy. * Worry that this patient will develop cor pulmonale. This is similar to CHF in a patient developing left ventricular failure due to hypertension. * Patient with COPD has obstruction so you hear increased wheezing, large AP diameter (barrel chest), and history including smoking, past episodes of bronchitis. * Patient with chronic bronchitis will have increased markings on chest x-ray. Patient with emphysema will have blebs that can become bullae, flattening of the diaphragm, widened silhouette so heart looks smaller, breath and heart sounds may sound very distant. * Pulmonary function tests will be diminished FEV1 and FEV1/FVC ratio. * DLCO test can help differentiate between bronchitic patient and emphysematous patient. There is destruction of the alveolar-capillary membrane in emphysema (low DLCO) but not bronchitis. * In an asthmatic, we give them beta2 agonists acutely and try to keep them well between attacks with steroids. * Ipratropium tends to work better in COPD than asthma for bronchodilitation. * Beta2 agonists help in COPD. Antibiotics for frequent bronchitic infections; They get pneumococcus, h. influenza, moraxella catarrhalis. We use sulfa antibiotics, penicillin antibiotics, cephalosporins, sometimes tetracycline. We try to rotate these antibiotics. So say patient had a good response to TMP-SMX; next choice when they get an infection should be something new else they will develop resistance, so ampicillin or erythromycin. Macrolides (azithromycin) and fluoroquinolones (levofloxacin) also good choices. * Aminophylline is a phosphodiesterase inhibitor with minor bronchodilation effect that has some use in COPD. Toxicities of aminophylline include tachycardia, tachyarrhythmias, tremors, and seizures. We have much better and safer bronchodilators in asthma, namely the beta2 agonists like albuterol. * Aminophylline used in COPD to increase central respiratory drive, improves diaphragmatic contractility, it makes the work of breathing smoother. * Say patient is long-time smoker and getting tachyarrhythmia. Next step is stop theophylline or aminophylline and get an aminophylline level. * Aminophylline is not cleared well in patients on erythromycin, ciprofloxacin, and cimetidine. Drugs that decrease aminophylline levels include warfarin and phenytoin. * Steroids should be monitors. Even with inhaled steroids patient can get cataracts, osteopenia, osteoporosis, hypertension, fluid overload, diabetes, and so on. Demonstrate benefit (baseline PFTs) pre- and post-steroids. * Most patients do not benefit from steroids if you do the measurements before and after a couple of weeks. * Most important treatment for COPD is stopping smoking. Even stopping smoking after decades of damage has benefit. Smoking cessation improves symptoms and mortality. Combine pharmacologic and counseling. * When is the patient hypoxic enough to get chronic home O2? Criteria is PO2 < 55mmHg at rest. If PO2 between 55 and 60mmHg, likely you will be less than 90% oxygen sats. So in this group, look for end organ damage, so erythrocytosis (Hct increased) as a compensatory mechanism or signs of cor pulmonale. * So how much oxygen? It’s cheap, why not just give 100%? These patients have respiratory acidosis, 7.30/50/50, so they have high PCO2, low PO2, “50/50 club.” Home O2 not only makes this patient feel better, it makes them liver longer. We want this patient into the low 90% oxygen sat range. We don’t want to knock out their hypoxemic drive to breath, else we’re in big trouble. This patient is already acidemic, so they need some hypoxia as a central CNS respiratory drive. Otherwise they hypoventilate more, PCO2 goes up, pH goes down. * Typical dose is home O2 1-2L via nasal cannula. * COPD patients should get pneumococcal vaccine every 5 years. They should get influenza virus vaccine annually. They can also get the hemophilus influenza (faintly staining gram negative rod) vaccine once in a lifetime. * What is the most important test for COPD? Answer is FEV1 as a measure of lung disease. -------------------------------------------------------------------------------------------------------------------------------------------Bronchiectasis * Destruction of the elasticity of the bronchial walls, leading to recurrent infections. * Bronchiectasis seen in chronic bronchitis patients and in kids with recurrent infections (tram track sign on chest xray), think about cystic fibrosis.
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Worry more about things like TB. so you expect a restrictive lung pattern (decreased PFTs. and nasotracheal suction. If no improvement. DO NOT DISTRIBUTE . finger clubbing (not specific. We don’t necessarily have information to know this is sarcoidosis. Kveim-Siltzbach) test is the equivalent of the PPD/mantoux test for TB. So FEV1 and FVC diminished but ratio of FEV1/FVC is the same. -------------------------------------------------------------------------------------------------------------------------------------------Interstitial Fibrosis * Almost always idiopathic. What is the next step in confirming diagnosis? * The painful red nodules on the shins are erythema nodosum. So either give steroids or refer immediately to the ophthalmologist for slit lamp exam. are ingested by macrophages.18 - . tuberculosis). * Pulmonary toilet (pulmonary hygiene) is helpful here too. * In asbestosis there is a synergistic cancer effect with smoking. * On chest x-ray with sarcoidosis. * Rarely will these patients respond to steroids. cor pulmonale. In cystic fibrosis. Generally no lung involvement in Crohn disease. seen in older patient. * Asbestos found in older building insulation. gold. Other causes of bilateral hilar adenopathy are granulomatous diseases (e. * These patients require the same vaccinations as in COPD. Postural therapy. temporal arteritis. PIP joints. copper. * Unilateral hilar lymphadenopathy not seen in sarcoid. -------------------------------------------------------------------------------------------------------------------------------------------Sarcoidosis * A 27yo woman comes to your office with painful erythematous papules that occurred one day before your visit. CNS involvement (treated with steroids). If they are a smoker. silver. so do a mediastinoscopy to biopsy nodes. Pneumoconiosis. PFTs similar to restrictive disease. and causes scaring over the years. you would think emphysema. The physical exam reveals low-grade fever. normal FEV1/FVC). blow bottles. * Pneumoconiosis seen in the mining industry or heavy metal exposure. * These patients are generally not smokers. lead inhalation. The papules are red and tender. * Other disease involving the head that can cause blindness. but implies chronic). * Hypercalcemia seen in sarcoidosis due to elevated levels of vitamin D so absorb more calcium. remove patient from environment if still there. Kveim test is a purified antigen from the granulomas of sarcoid patients.Study Notes – Internal Medicine James Lamberg 28Jul2010 * Be aggressive with pulmonary physical therapy. and MCP joints. * Kveim (Nickerson-Kveim. Add in joint swelling and we could be talking about Crohn disease. hypercalciuria too. boilers. not helping to brush out infection. have patient quit smoking. parotid gland enlargement. want biopsy. infection is likely to be pseudomonas aeruginosa. * Diagnosis is with tissue. then stop the steroids. * Sarcoid causes scaring. She has no other complaints except joint swelling and pain that occurred three days ago. pneumococcal. bilateral lymphoma. hemophilus influenza. Could biopsy supraclavicular node if it is available. pipes. photophobia. * Pneumoconiosis comes with opacities and irregular densities on CXR. uveitis (ocular emergency requiring steroids). Measure pre-steroid PFTs and post-steroid PFTs. Chest x-ray will show increased white markings (from scars). * Sarcoid associated with Bell palsy. silicosis. -------------------------------------------------------------------------------------------------------------------------------------------Occupational Lung Disease * Typically occurs 10-20 years down the road. liver granulomas with elevated LFTs. * No good treatment. have them bend over. asbestosis. * Patients may develop episodes of blood-tinged sputum or hemoptysis. pain in the eyes. Also have immotile sperm. Tissue should show non-caseating granulomas. clap on their back to get mucus moving. * Sarcoid more commonly seen in younger patients and in African American patients. This is dextrocardia with situs inversus. shipyard workers.g. erythema nodosum on the lower extremities). nickel. This is immotile ciliary syndrome. all volumes are diminished. with well demarcated 3-4cm papules over the anterior aspects of the legs. * Smoking exacerbates and is superimposed on these diseases. “ground glass” appearance. skin lesions (lupus pernio on face. What PFTs would you expect? Pattern is similar to restrictive. cancer. suctioning of the airways. This causes a chronic inflammatory response. influenza virus. old building construction. chest physiotherapy. bilateral hilar lymphadenopathy leading to lung scaring and eventually honeycombing pattern. * Patients may have angiotensin converting enzyme (ACE) elevations. * On exam you find pulmonary hypertension. not sensitive or very specific. you see bilateral hilar lymphadenopathy. metastatic adenocarcinoma. This is not a test of choice. Think Kartagener syndrome (primary ciliary dyskineasia). and metastasis. symmetric swelling of the knees. and coal worker’s lung. * Uveitis usually occurs rather abruptly. * Given a chest x-ray of a bronchiectasis patient where you see the liver impression on the right and gastric airbubble on the left. * All have a restrictive lung pattern so come with decreased PFTs.
you know it is likely a question about pulmonary embolus. * Patients at risk for DVT get anticoagulated (subcutaneous heparin) or get sequential compression devices (SCDs). * To detect a V/Q mismatch. or moving) that occurred while she was shopping. * What is the quickest test to determine if a patient needs treatment for a PE? Answer is Doppler. This is rarely necessary. you order a V/Q scan. intermediate. pH goes up by 0. then you do the pulmonary angiogram. Restrictive disease. But there is a clot blocking blood in the pulmonary artery. -------------------------------------------------------------------------------------------------------------------------------------------Pulmonary Embolism (PE) * A 32yo woman is brought to the ED with acute onset shortness of breath and pleuritic chest pain (sharp pain. you should think about rheumatoid arthritis (Kaplan syndrome) and check rheumatoid factor. spiral CT scan. * In a PE. 5000U subq q12h) as well as post-op anticoagulation. Primarily you see thick pleural bases. Other hypercoagulable criteria are not included in Wells. * Gold standard to detect a PE is a pulmonary angiogram. An embolus is a broken off clot that traveled. thighs > calves. clinical signs/symptoms of DVT. CXR nodules favor the upper lobes (similar to TB). thing PE. * Silicosis is seen with rock mining. Normally there is a superimposed pattern of ventilation and perfusion. ventilation/perfusion (V/Q) mismatch. ABG 7. * Another non-invasive test is a Doppler sonogram of the lower extremities. is tachycardic. * Patients develop interstitial lung disease. Say the Doppler is equivocal and the V/Q scan is equivocal. * Gold standard to determine if a patient has a DVT is a venogram. With intermediate. * CXR shows calcification of the pleura (white areas). PE is likely #1 diagnosis. If you happen to get a biopsy. waste of ventilation. there will be barbell shaped ferruginous body (asbestos fiber coated with iron-rich material). Detected by biopsy only. * Treatment is to get patient to stop smoking. * Coal miner’s lung associated with mining coal. So the problem is with gas exchange. no wheezing. * 70-fold increase in primary lung cancer in asbestos exposure with concurrent tobacco smoking. previous PE/DVT. * A-a gradient: 150 1. especially hip replacement). So you need to do testing. ABG shows mild evidence hypoxemia. digging quarries. * V/Q scan is not gold standard. She has never been sick before. * Patients with silicosis should get annual PPD testing. * A Doppler is a valid initial approach in a pregnant patient. The test is painful. If there is a PE. nearly always fatal. and hemoptysis. * Encourage patient to quit smoking. small round densities typically mid to lower lobes. it is likely too late.Study Notes – Internal Medicine James Lamberg 28Jul2010 * No specific signs or symptoms. you will see ventilation but no perfusion in a particular area. only done if you have no choice. * Mesothelioma is a specific and rare cancer seen with asbestosis.75 = 45 (normal < 15). post-op. * Pulmonary angiograms are used less widely now due to more acceptance of the spiral CT scan with contrast.g. Results come as low. * Restrictive disease. ventilation perfusion scan. diagnosis found via occupational history. * What is the first step in detecting a pulmonary embolus? Answer is V/Q scan (non invasive study). * Risk factors for pulmonary embolus (Wells criteria): immobilization (e. Her respiratory rate is 26.08. the alveolus is just fine. eggshell white. * By the time you think to biopsy a cancer. worse with deep breath. such as symmetric swollen joints possibly with hand involvement. the airway is just fine. * A thrombus is a clot at its point of origin. If there is a blood clot. injection of dye into small vein of the foot with imaging to see the dye. The radiologist has a large list of criteria to determine probabilities.52/25/75. * The DVT risk for hip surgery is so high that standard of care includes pre-op prophylactic anticoagulation (subcutaneous heparin.2*25 = 120. So there is an area that is ventilated but not perfused. * Patient may be ambulatory but have dementia so they don’t leave bed. * Patients with coal miner’s lung who have joint complaints. HR > 100. Patient breathes in nuclear-labeled air and an image is taken to determine ventilation. digging tunnels. such as use of oral contraceptives. since the presence of DVT warrants anticoagulation. Answer is not mesothelioma.19 - . cancer. lungs are clear. This patient is not taking any medications except oral contraceptives. * What is the most likely type of lung cancer a patient with asbestosis will get? Answer is adenocarcinoma or squamous cell carcinoma primarily of the lung parenchyma. especially if a smoker. * If you see oral contraceptives (hypercoagulability due to estrogen) and sudden chest pain. that is enough to start with anticoagulation. Silica fibers are released from rock blasting. DO NOT DISTRIBUTE . use subcutaneous heparin. rest of exam is normal. These patients are at increased risk for TB. no rhonchi. If you look down and see answer choices like venous Doppler. Then IV nuclear material is labeled to RBCs and another image is taken to determine perfusion. or high probability of PE. * Physical exam will reveal an absence of problems. coughing. So 120 . you may be forced to do more tests. Drop PCO2 by 10. A PE usually originates from the deep veins of the legs or pelvis.
recent major trauma. then we can start the warfarin. a qualitative problem. this is most likely a PE case. has a baby pressing on her pelvic veins. Problem with PT test is control time varies too much. Factor V Leiden causes activated protein C resistance. Prothrombin no longer measured directly. So you want to prevent the clot from getting bigger. Heparin is safe during pregnancy. Start patient on oral anticoagulant (warfarin/coumadin) that they will stay on for the next 3-6 months. If for stroke or prosthetic valve. * Treat patient with IV heparin for about 5 days. * Heparin works by potentiating antithrombin III effect.20 - . So we treat the patient with IV heparin for 5 days then send them home on subcutaneous heparin (10.000U subq TID as we need 20k to 30k units daily). IX. right axis deviation on ECG. think hypercoagulable state. which will work within the hour. Examples are recent major surgery. Treatment is anticoagulation. * Clots in strange places. If PTT low. recent duodenal bleeding ulcer. Protein C has the shortest half-life. you want 45 to 75 seconds. * If the pulmonary embolism makes it peripheral to the pleura. Pregnancy increases risk for DVT. * Low molecular weight heparin (LMWH) has more consistent effect on PTT. * FFP comes from other human beings thus it can come with infections and transfusion reactions. So if INR is 1. or ECG S1 Q3 T3 pattern (abnormal S wave in I. IX. * If a large pulmonary vessel is clotted. Warfarin inhibits protein C. even with a massive PE the CXR will be normal. stop heparin for a few hours to let the level come down as patient is at high risk of bleeding. and flipped T wave in III. * So once PTT is 1. you can get signs of right ventricular strain. So. VII.5 to 2. Q wave in III. Oral vitamin K will lower INR in 24-48 hours. If this patient does get a DVT. like upper extremities (axillary vein) or in any artery. the pleura can infarct and cause a pleural rub.Study Notes – Internal Medicine James Lamberg 28Jul2010 * Patient is normally ambulatory busy businessman. May see signs of cor pulmonale acutely. INR between 3-4. so it will not break the clot. increase heparin infusion rate. antithrombin III) to break up the clot and after time the vessel will recanalize. Once the patient has a stable PTT. * We do not start warfarin at the same time as we start the heparin. * Warfarin works by inhibiting vitamin K dependent coagulation factors (II. still in the presence of a clear lung exam. * Drug interactions are important with warfarin. * Warfarin has a sizeable morbidity and mortality associated with it because there is variation in week-to-week or even day-to-day dosing. so much so that we do not need to follow repeated PTT levels. IV vitamin K will lower INR in 6-8 hours. we just follow the dose. not specific or sensitive). Warfarin is contraindicated in pregnancy. we give factors II. Keep patient on continuous heparin infusion. If control in assay is 30 seconds. * A patient has a positive V/Q scan with symptoms. If INR is 5. * When do you need to know for sure that this is a pulmonary embolus. This is not the normal case. we need to reverse the effect of warfarin. takes long flight across seas and is suddenly short of breath. * If the patient has a high INR without bleeding. VII. this patient got pregnant and now is hypercoagulable due to estrogen. Subcutaneous vitamin K not recommended. recent CVA. P2 louder with inspiration. so they have more tendency toward hypercoagulability.5-2. “pro time”). * Check heparin level with PTT (partial thromboplastin time) test. International normalized ratio (INR) range for a DVT is between 2 and 3. So.5 times control.5 times the control. She has been gaining weight and stays at home most days. * Factor V Leiden is the most common cause of thrombophilia. give vitamin K. Heparin is not thrombolytic therapy. it is teratogenic. plus protein C). we have to regularly check INRs. LMWH is a once a day dose. it is done by INR. and is not moving around much. so much so that you do the invasive and possibly risk pulmonary angiogram or pulmonary venogram? You do it when patient is at very high risk of bleeding if you anticoagulate them for treatment of the PE. more specifically fresh frozen plasma (FFP). If you’re at a PTT of 100. protein S. then we can give heparin. You expect the patient’s own endogenous system (protein C. * Patients with CHF are at increased risk for DVT/PE due to poor cardiac output and blood stasis. DO NOT DISTRIBUTE . * Measure warfarin via PT (prothrombin time. distended neck veins. as many drugs affect the same P450. loud S2. shorter than factor VII. You could see this on CXR possibly. Factor V is necessary for protein C to work. so quantitative levels of protein C are normal. X. Even sitting in a car for a long trip. acute right ventricular heave. * The problem with LMWH is that they are very expensive. * If patient bleeding with high INR. could be a few hundred dollars a day. X. The fastest acting anticoagulation agent is IV heparin. Heparin is given in bolus (say 5000U) then infusion (say 10 or 15U/kg) at say 1000U/hour.7. increase oral warfarin dose to get them above 2 for the DVT. So the first effect warfarin has is to make the patient protein C deficient. Aiming for time of 1. You do not think the patient is going to die from this clot. Protein C and S as well as antithrombin III (AT III) are necessary to prevent constant coagulation. * 25yo woman stopped taking her birth control pills because she is scared of clots after reading about them on the Internet.
but anticoagulation is contraindicated (e. * Say patient had major PE then became hypotensive and fell. we diagnose and treat with the correct PTT then INR. burns. real 60% oxygen into trachea with patient intubated.g. * ARDS also known as non-cardiogenic pulmonary edema. you increase right-sided venous return at the expense of the left ventricle. * Why don’t we just give tPA in every patient? About 1% of patients getting thrombolytics die of a bleed. * ARDS occurs in gram-negative sepsis. pulmonic valve. thus we do not stop the anticoagulation if we do not have to. insert a pulmonary artery catheter (Swan-Ganz catheter). For instance. * Treatment for life-threatening PE is thrombolytic therapy. the right ventricle is trying to pump against tremendous resistance. which causes fibrosis. so it will acutely fail. In less common instances. PEEP holds the alveoli open. but can’t anticoagulate. SVC filters can be placed as well. This causes a ventilation perfusion mismatch at the entire lung. a post-op patient who got a DVT or a patient who got a DVT after a plane ride. into outflow tract with balloon deflated. * Risk of giving PEEP is blowing a hole in the alveolus. Diffuse alveolar densities are seen on CXR. which helps to force the air through the fluid. So even if you intubate the patient and deliver 100% O2 directly into the trachea. An ABG shows hypoxemia and hypercarbia. Do you give tPA or streptokinase? Answer is emergently take patient to the OR or via interventional radiology (IR) to do an embolectomy. and patient getting hypotensive.Study Notes – Internal Medicine James Lamberg 28Jul2010 * Say patient has life-threatening PE. * Patient on ventilator. Or patient has major PE and a recent GI bleed. drowning. barotrauma. Definition is PO2 < 60% on FIO2 > 60%. * Treatment is intubation and delivery 100% inspired oxygen. DO NOT DISTRIBUTE . This will lyse the clot. so oxygen cannot diffuse through the fluid to the membrane. mediastinum shifts away. * One sign this is a potentially fatal PE is that we are delivering 100% oxygen and the sats keep dropping. causing pneumothorax. Inflating the balloon too much could rupture the pulmonary artery. like CHF or an underlying coagulation disorder? Then we anticoagulate for as long as the risk exists. like internal jugular or subclavian (IJ safer because further from lung). Some IVC filters are shaped like an umbrella (IVC umbrella). you have to rule out cardiac so normal pulmonary wedge pressure and LV end diastolic.21 - . About 10% of patients getting thrombolytics have a major bleed. Answer for next step is to decrease PEEP. the PEEP will continue to push air out. We have to protect the patient against future emboli. trauma with or without multiple PRBC transfusions. * We anticoagulate the embolus 3-6 months if there is a reversible cause. The patient seems to improve over the next day. * To measure capillary wedge pressure (PCWP). is hemodynamically stable. RV. resulting in an intracranial bleed. Hypotension in the setting of pulmonary embolus is an ominous finding. * Oxygen toxicity can occur with FIO2 > 50%. What about patients who have an on-going risk. Blood cultures grow pseudomonas sensitive to ceftazidime and ciprofloxacin. If an ABG shows PO2 low (like 45). * Thus to prove ARDS. others may be mesh patterned. some are disk shaped with pores. Give tissue plasminogen activator (tPA) or streptokinase (SK). which the patient has already been started on. Say patient got a DVT in the first month of pregnancy due to increased estrogen levels. then we add PEEP (positive end expiratory pressure). Catheter placed through RA. The lungs are flooded with fluid. The filter itself is thrombogenic. So we put in an inferior vena cava (IVC) filter. if there is enough time to save the patient. compared with an unremarkable admission chest x-ray. narcotic overdose. then we anticoagulate for the entire pregnancy. He is placed on double gram-negative antibiotic coverage and remains stable for the next 24 hours. resulting in hypotension. so we can measure the pressure in the pulmonary artery. Insert into a large vein. left atrium has no input thus no LV output. * Say the patient has a PE. like a saddle embolus at the main pulmonary artery. so think of it as compressing the left ventricle. * Giving these patients oxygen does not do much to fix hypoxemia. * As intrathoracic pressure gets increased with PEEP. no blood will be there to transfer the oxygen into the system. What if the patient gets another pulmonary embolism? Answer is place an IVC filter. -------------------------------------------------------------------------------------------------------------------------------------------Acute Respiratory Distress Syndrome (ARDS) * 32yo man is admitted to the ICU with presumed gram-negative sepsis. until he suddenly develops severe dyspnea. CXR normal. Another sign is acute right ventricular failure with hypotension. Physical exam reveals diffuse crackles. * Premature newborns get similar problems (gas exchange problem at the alveolar-capillary membrane) when born without enough surfactant. or blood gas shows increasing hypoxemia. leading to a tension pneumothorax. * What if the patient has a PE. On the catheter is a pressure transducer. recent major hemorrhage). * If you cause a pneumothorax and do not recognize it. Patient will become hypotensive.
The quickness and degree to which the temperature falls in response to the saline helps determine the rate of flow and thus the cardiac output (L/min depending on BSA). 3rd is colorectal. CXR 3 weeks later still shows a patchy spot. -------------------------------------------------------------------------------------------------------------------------------------------Lung Cancer * Most common cause of cancer death in both men and women is lung cancer. * Chronic smokers generally develop chronic hoarseness/laryngitis. It is not a popular test because the patient is trying to fall asleep while hooked up to all these devices. Thermometer tells you what the temperature of the blood is. it travels down and gets wedged in the pulmonary capillary. the mitral valve is still open so the pressure is transmitted back to the left atrium.22 - . respiratory rates measured. post-obstructive pneumonia. * A non-smoker that gets lung cancer is likely adenocarcinoma. blood-tinged cough. nearly all are unresectable. * Cardiac index should be > 2. * Say LVEDP normally is 7-12mmHg. so this is the left ventricular end diastolic pressure. * Women: 2nd cause is breast cancer (1st if non smoker). ECG. * We have no good diagnostic test to improve survival in smokers who develop lung cancer. Below 2. 5-year survival rate is about 5%. * Seen in obese patients. * The positive pressure in CPAP is being delivered to the mouth. * Cough with another symptom. Maybe they have superimposed bronchitis. So pulmonary edema with low LVED pressures suggests ARDS. If not cleared. which is in continuous communication with the left ventricle. not always successful. * Once a patient has about 10% weight loss with a new lung cancer diagnosis. * Cardiac index may be normal or high in ARDS. * Testing done in sleep lab. We get a continuous column of pressure at that capillary. * So we inflate the balloon. smokers usually cough. So. * Say pulmonary capillary wedge pressure (PCWP) is 25mmHg with edema? That is cardiogenic. this implies unresectable cancer. * So any smoker with pneumonia you must follow CXR until it is clear. Take chilled saline that you know the temperature and fluid amount. similar concept as PEEP. Testing is with laryngoscopy and patient phonating to determine if a vocal cord is paralyzed (ENT consult). -------------------------------------------------------------------------------------------------------------------------------------------Sleep Apnea * Sleep apnea is cessation of breathing during nighttime sleep. * You can also measure cardiac output via the Fick equation with a Swan-Ganz catheter. occurring at least 10-15 times per hour and at least 10 seconds per episode. * Major cause of sleep apnea is obstruction of the upper airway at the larynx and epiglottis. That is because secretions cannot clear due to obstruction. * Superior vena cava syndrome implies a big mass in the chest is impinging the SVC. drink more and more coffee and still falling asleep. Associated with paraneoplastic syndrome of hypercalcemia due to parathyroid hormone like substance secretion. you should worry that metastasis has traveled to the recurrent laryngeal nerve (outside lung). * You can follow cardiac index to help determine how much diuretic or inotrope to give. * Catheter has a thermometer on the tip along with balloon and pressure transducer. so no risk of barotrauma like in PEEP. Taking all lung cancers that present to the physician’s office.2 is very poor flow. * Men: 2nd cause is prostate (1st if non smoker). falling asleep while driving) or spouse notices loud snoring. * Most common initial presentation is a cough. * If the lesion is somewhere in the middle. look for a change in the cough. patient hooked up to EEG. * About 5% of cases are central apnea where the issue is not in the upper airway but in the respiratory drive. the ventricle is maximally full. must get bronchoscope. * If cancer is found and centrally located. like pleuritic chest pain.2 L/min/BSA. If a patient suddenly develops hoarseness. so more likely to be bronchoscopy with biopsy. you can do a bronchoscopy and biopsy. * Treatment is with CPAP (continuous positive airway pressure) mask at night. but in cardiogenic pulmonary edema it is low. * More invasive treatment if CPAP fails is surgical intervention to open the airway. what if the pressure is 5mmHg? The low pressure suggests it is noncardiogenic pulmonary edema (ARDS). This is a very non-specific symptom. aortic valve is closed. must do an open biopsy (can be done laparoscopically these days). Will have tremendous intolerable (to others) snoring. This is a difficult diagnosis at times. that pressure transmits back to the pulmonary veins. You inject the saline and the catheter measures continuous temperature. Patient gets pneumonia. * Post-obstructive pneumonia is when patient has recurrent pneumonia in the same location. * Patient does not realize this is happening. and back to the pulmonary capillary.Study Notes – Internal Medicine James Lamberg 28Jul2010 * At the end of diastole. Patient will get swelling in face with redness. DO NOT DISTRIBUTE . * Squamous cell carcinoma is generally centrally located. called facial plethora (Pemberton sign). pulse ox. So either the patient has daytime somnolence (fall asleep at my desk. * If the lesion is peripherally. gets better. one can do a CT guided needle biopsy. 3rd is colorectal cancer.
esophagus). The questions are not meant to trick the test taker. poor cardiac output especially CHF). you should worry about outlet obstruction. So by the time you make the diagnosis. * Pre-renal azotemia is due to poor perfusion of the kidney. Barry Weiss. Causes include volume depletion (dehydration. papillary necrosis). If untreated. best considered as transient ischemia. Lab tests show creatinine of 3. local extension into nearby organ. ACE-I. but 95% are not cured at 6 months and die. Post-renal could also have a BUN/Cr of 10-20. * Small cell cancer metastasizes early. and post-renal azotemia (outflow). pelvic tumors. so if a post-void scan shows 300mL of urine. such as a large tumor causing obstruction. To determine if the patient can be cured. we’re talking about Lyme disease. but this is not a cure. functional kidneys retain sodium to maintain vascular volume. you must assume there has been micro metastasis and thus resection is not an option for cure. * Tests for post-renal azotemia include prostate exam. early SVC syndrome. Why are the kidneys failing? * Three main causes of acute renal failure: pre-renal azotemia (non kidney problems. * Adenocarcinoma carcinoma and large cell carcinoma tend to be more peripheral. best test is ultrasound of the kidneys. < 10 is intra-renal.g. * In low-flow states. * Patients may still be resected for palliative measures. * Even if you have a tiny lung cancer and a single node on the contralateral mediastinum. thus urine sodium is very low. Eaton-Lambert syndrome. urethral stricture). functional kidneys will concentrate urine to retain fluid in the body. There are similar key words and patterns to know for nephrology. * What happens is the kidneys don’t get enough blood. associated with SIADH (hyponatremia with euvolemia). and anatomic like renal artery stenosis). renal artery vasoconstriction (meds like NSAID. * 62yo man comes to the ED for nausea and vomiting. -------------------------------------------------------------------------------------------------------------------------------------------Acute Renal Failure * If you’re told a patient has bad breath.6. Signs of metastasis would be malignant pleural effusion.23 - . (< 1%). catheterization or bladder scan (to detect post-void residual urine volume). liver. * Eaton-Lambert syndrome is neuromuscular end-plate injury. so high (concentrated) urine specific gravity and high (concentrated) urine osmolality. ureteral obstruction (tumors. can progress to renal damage (acute tubular necrosis) and intrinsic renal failure. or FENa. -------------------------------------------------------------------------------------------------------------------------------------------Kaplan Videos (2001) – Nephrology with Dr. look for lack of metastasis. bone involvement. so they retain lots of sodium to help build up intravascular volume. straightforward topics with obvious answers if you know the content. intra-renal azotemia (intrinsic disease). * The only good news about lung cancer is the rates are decreasing as people are smoking less and less. brain involvement. burns. * Non-small cell lung cancer can be palliated with chemo and radiation. A canoe trip in Connecticut. * Post-renal azotemia causes include bladder outlet obstruction (prostate enlargement. * Normal BUN/Creatinine ration is 10 to 20. you can be sure we’re talking about Zenker diverticulum. These are classic cases. * The greatest impact to reduce lung cancer rates is through education of teenagers before they start smoking. decreased oncotic pressure (low albumin edematous states like cirrhosis. * Tests for pre-renal azotemia include high BUN/Cr ratio (> 20) is the most important. Significance is back pressure damages kidneys.Study Notes – Internal Medicine James Lamberg 28Jul2010 * Small cell (oat cell) carcinoma generally centrally located. stones. DO NOT DISTRIBUTE . it was normal two months ago. and bladder (U/S KUB). differentiated from myasthenia in that muscles improve with use (MG patients worsen with use). In low flow states. so needle aspiration biopsy or thoracotomy to get tissue for diagnosis. * You can have local nodes and be cured with resection only if the nodes are on the same side of the cancer. MD -------------------------------------------------------------------------------------------------------------------------------------------Questions should be core. classic scenarios. * Intra-renal failure is damage to the kidney itself. nephrotic syndrome). * Non-small cell cancers can only be cured if they are resected prior to metastasis. * One could be cured with chemotherapy in small cell cancer. third-spacing into abdomen from pancreatitis). inflow issues like circulation). * Some of the blood flow into the kidney is prostaglandin-dependent and NSAIDs block prostaglandin. so low urine Na+ (< 10-20) and low fractional excretion of Na+. cardiovascular (hypotension. it’s too late to cure. ureters. local contiguous structures (e. * You expect about 50mL of urine left in bladder after urination. also called intrinsic renal disease or acute tubular necrosis (ATN). * Must be distinguished from intra-renal and post-renal azotemia because the treatments are very different. they think you are bleeding to death (evolutionary response). * Pre-renal azotemia is important because it represents low blood flow to the kidneys.
Signs of intra-renal disease are BUN/Cr < 10. methotrexate. * Elderly man dropped pen under bed and went to go retrieve it. you’re faced with a high creatinine level that is new (azotemia). urine osmolarity < 350. hypertension. * Phases of ATN are prodromal. * Infection causes include pyelonephritis with WBC casts and bacteria in urine. The broken down muscle tissue releases myoglobin. penicillins). -------------------------------------------------------------------------------------------------------------------------------------------Intra-Renal Disease: Tubulo-Interstitial Disorders * Acute tubular necrosis (ATN) occurs in prolonged ischemia (hypotension. Answer to why they are failing is pre-renal azotemia. Had a sore throat a week before. granular and RBC. cephalosporins. * Nephrotic syndrome occurs in vasculitis and glomerulonephritis. and ANCA anti-neutrophil cytoplasmic antibodies). cryoglobulin disease. BUN/Cr is high. or treat CHF or renal artery stenosis). arterial insufficiency/occlusion. cephalosporins. drugs like aminoglycosides and amphotericin B. * Glomerulonephritis causes include post-streptococcal (do ASO titer. rifampin.015. If you find post-renal. which goes through the renal tubules and is toxic to the tubules. amphotericin B. antibiotics (aminoglycosides. Alport syndrome (renal failure and deftness). radiation nephritis. thrombotic thrombocytopenic purpura. prolonged pre-renal azotemia. * Algorithm: First thing to do is exclude pre-renal azotemia by looking for lack of BUN/Cr > 20. Neighbor realizes man hasn’t come out of the house for a few days and finds the man stuck under the bed.Study Notes – Internal Medicine James Lamberg 28Jul2010 * 62yo man comes to the ED with nausea and vomiting. young children). follows strep skin or throat infection). oxalate crystals (ethylene glycol.5g/day. RBC casts). -------------------------------------------------------------------------------------------------------------------------------------------Intra-Renal Disease: Glomerular Disorders * Vasculitis causes include Wegener granulomatosis (lesions in lung. this is 4+ dipstick positive with grams on measurement. Osm > 500. expired tetracyclines leading to Fanconi syndrome). allopurinol. collagen vascular disease (e.g. Can’t concentrate urine. hypercalcemia (hyperparathyroidism). Next thing to do is exclude post-renal azotemia by sonogram and/or catheter looking for lack of obstruction. rash. pigments like myoglobin). * Patients who have diabetes (and are taking metformin) and get contrast dye should have the metformin stopped prior to the procedure. Also look for casts. Treatment is stop drug and short-term steroids to cool down reaction. previously called “shock kidney”). heavy metal poisoning (lead. Think Wegner and order ANCA.6. high specific gravity. * Allergic interstitial nephritis is an allergy reaction to a drug. polyarteritis nodosa. gold. urine specific gravity 1. mercury. * Patient has lung lesions and recurrent sinus infections. gout). * Treatment for pre-renal azotemia is fluids. FENa < 1%. creatinine was normal now is 2. it is most likely intrinsic renal. * In summary. Key findings are urine eosinophils. Has orthostatic hypotension. Urine sodium >20-40 because kidneys are failing so they lose the ability to protect sodium. Presentation is fever. DO NOT DISTRIBUTE . If you find pre-renal.g. cancer drugs (cisplatin. tumor-lysis. These patients will lose their oncotic pressure and develop edema. Answer is order ASO titer. sulfonamides. * If patient on diuretics. BUN 82. * Teenager presents with intrinsic renal disease. * Intra-renal azotemia: BUN/Cr is < 10-15. * Deposition disease causes include hemoglobin (hemolysis). treat it. like furosemide. cyclosporin.24 - . low specific gravity. So. Berger disease (IgA mesangial deposition after viral illness. abnormal urinary sediments (hematuria. urine Na > 20. Henoch-Schonlein purpura. Also has kidney issues. oliguric (when kidney starts showing changes). FENa > 1%. toxins (radiologic contract. Massive proteinuria > 3. vitamin C). it just leaks out. Renal biopsy is the most definitive test. uric acid crystals (chemotherapy. so urine specific gravity < 1. Once uncer the bed he couldn’t get out. If you see urine eosinophils. * Drugs and toxin causes include analgesics (NSAIDs). then that may cause high urine sodium do don’t assume intra-renal failure. urine Na+ 6. Goodpasteur syndrome (anti-GBM antibodies in lung and kidney). if you don’t see pre-renal or post-renal problems. nasal. Typical drugs are beta-lactams (e. protein (multiple myeloma with Bence Jones protein). Follow azotemia algorithm. not done often in clinical practice because of risk. diabetes. in intra-renal BUN/Cr is low with high urine sodium. Osm < 200. think allergic interstitial nephritis and look for what drug needs to be stopped. Patient has been lying on the big muscles of the legs for a long time with no good circulation. sinus.028. myoglobin (rhabdomyolysis). SLE). * So in pre-renal BUN/Cr is high with low urine sodium. urine Na < 10. you treat the cause (most causes you give them fluid. and post-oliguric (diuretic). peripheral eosinophilia. -------------------------------------------------------------------------------------------------------------------------------------------Glomerulonephritis * Intra-renal disease has high urine sodium (> 20) and high FENa (> 1%). Casts come from the kidney. urine sodium is low so kidneys are retaining it. mitomycin C). lithium). most commonly a cephalosporin.
Exam is normal except large prostate. Metabolic acidosis occurs but kidneys cannot compensate. So pre-renal azotemia. Urine Na+ 9. not furosemide for CHF. Creatinine is 3. so need dialysis. Heavy proteinuria. no medications. think nephrotic syndrome. creatinine 3. What is the next step though? Answer is sonogram to exclude post-renal azotemia. drug hypersensitivity (eosinophils). start to occur when the creatinine gets to about 3. * Urinalysis can show infection (WBC. ECG shows tall peaked T waves. * Most common causes are diabetes (30-50%). BP 140/90 (pretty high). * Best initial test to distinguish causes of intrinsic renal disease is a urinalysis. BP 110/70. polycystic kidney disease (5-10%). high creatine kinase CK in blood). Patient has high pulse and nausea with vomiting. the combination of accelerated hypertension and hyperlipidemia leads to accelerated atherosclerosis leading to cardiovascular disease. so likely dehydrated. Hyperlipidemia also seen. pulse 110. exam confirms edema.023. If you look at the BUN/Cr. Eosinophils in urine. * Best test to determine the type of glomerulonephritis causing the nephrotic syndrome is renal biopsy. nephrotic syndrome (lots of protein). Best test to establish a diagnosis of nephrotic syndrome is 24-hour urine protein. BUN 41. but still need to rule out post-renal. There is a lack of 1. Pruritus occurs presumably due to toxins circulating in the blood that are normally excreted by the kidney. bicarb is 16 (metabolic acidosis). needs dialysis.2. Accelerated hypertension (renin-angiotensin action) occurs and is a big deal because it may be hard to control blood pressures. not to mess around with other treatment. Creatinine is 5. * Dialysis can be done via blood (hemodialysis via a machine) or peritoneal dialysis (fluid instilled into peritoneum then removed). Anemia occurs due to lack of erythropoietin production in the kidneys. can’t dilute urine even though he is vomiting/dehydrated. no casts. Urine shows proteinuria and RBC casts. but a 62yo man probably has a large prostate due to BPH. * Chronic manifestations of ESRD occur whether or not you are on dialysis. Could have BPH or cancer causing large prostate obstruction. not bicarbonate for acidosis.6 (new) and is on NSAIDs. * 62yo man comes to the ED for nausea and vomiting. What blood test would be most helpful for confirming diagnosis? Answer is ASO titer. He has a recent sore throat. BUN/Cr is close to 10. Hypocalcemia with osteopenia occurs. BUN 72. * 14yo boy comes to see you with swollen hands and legs. pulse 110. hypertension (10-25%). This is a clue up front because most people on dialysis get it every 2-3 days. urine sg 1. Immunosuppression occurs so increased infections. Urine sg 1. Dipstick is positive for protein and patient has edema. myoglobinuria (blood on dipstick due to myoglobin. needs dialysis. * 62yo man comes to the ED with nausea and vomiting. Urine Na+ 42. Could have hypoperfusion due to NSAIDs. glomerulonephritis (RBC casts). -------------------------------------------------------------------------------------------------------------------------------------------End Stage Renal Disease (ESRD) * ESRD is renal failure that is incompatible with survival. * Some key words in renal disease to remember. and can lead to them being obtunded and even comatose. Once that is out of the picture. no RBCs. it’s 20 plus concentrated urine. Hypermagnesemia occurs due to failure to excrete magnesium. myeloma (Bence Jones). Best initial treatment is fluids. So we ruled out pre-renal with urine originally. What is the best treatment for this patient? Answer is dialysis now. You see blood in the urine and RBC casts. so must get dialysis. * 62yo dialysis patient returns from a 4-day fishing trip and feels poorly. Pericarditis occurs due to toxins causing inflammation of the pericardium and build-up in the pericardial sac of fluid. BP 11/70. bacteria). * Need for dialysis is not determined by creatinine level. How do you prove it is nephrotic? 24h urine protein. RBC casts. calcium is leached from bone causing osteopenia. In order to survive. Fluid overload occurs to the point of pulmonary edema and the kidneys cannot remove the fluid. glomerulonephritis (15%).004. the mnemonic used is “the T-waves are so sharp and pointed that you don’t want to sit on them” meaning do not sit and wait before treating. * Acute manifestations of ESRD include hyperkalemia (look for peaked T-waves on ECG). This is likely intrinsic kidney (intra-renal) azotemia. High triglycerides think nephrotic DO NOT DISTRIBUTE . RBCs.Study Notes – Internal Medicine James Lamberg 28Jul2010 They can run their total albumin way down and get anasarca (“marshmallow man” appearance).6 (new). This is an indication for dialysis.25-dihydroxy vitamin D. What is the best initial treatment? You may be tempted to pick sonogram due to outlet obstruction. not kayexalate for potassium. Cardiac exam shows peripheral edema and signs of CHF. uric acid (gout). Exam normal except large prostate. and unknown (10-15%). and shortness of breath. Most common cause of dialysis is diabetic kidney disease. You rule-out pre-renal and post-renal. vomiting. This is post-streptococcal glomerulonephritis. we assume renal disease and follow that.25 - . It is determined by the presence of acute manifestations. Patient has nausea. Encephalopathy occurs at to high creatinine levels. usually asymptomatic. you need dialysis or a transplant. afebrile. think drug reaction like cephalosporins. All acute manifestations are indications for dialysis. think glomerulonephritis. This causes secondary hypoparathyroidism. * So you have a patient with azotemia. which is involved in calcium reabsorption in the GI tract. Could have bladder cancer or kidney stones due to RBCs in urine.
normal volume states. May be a drug side effect. and hyponatremia with low osmolality (true hypoglycemia. * Patient presents with weakness.Study Notes – Internal Medicine James Lamberg 28Jul2010 syndrome. Serum osm is 292 (normal). think pre-renal give fluids. including cirrhosis and congestive heart failure. Radiologic contrast. Blood osm is low/dilute. salt-wasting nephropathy (renal failure). symptoms include headache and confusion. * Hyponatremia with high osmolality caused by increase solute in the blood. glucose is 142. Say glucose is 342 and sodium is 126. If ECF is low (hypovolemia). -------------------------------------------------------------------------------------------------------------------------------------------Electrolyte Disorders: Hyponatremia * Hyponatremia is arguably the most common of the sodium and potassium abnormalities seen in the hospital. multiple myeloma). * Causes of SIADH include lung disease. We have low sodium with normal osmolality. If the ECF is normal (euvolemia). hyponatremia with normal osmolality (high lipids or protein). Extrarenal loss (urine Na+ < 10) due to GI loss from vomiting.6 is 4. * Low osmolality with hypervolemia. In this case. showing hyponatremia (diluted) and hyperglycemia (from the dextrose). water intoxication (> 12-20L/day. * Hyponatremia algorithm: once we rule out high osmolality and normal osmolality. tube drainage. where sodium level measures low but artifacts from other substances make it appear low. the patient is fluid overloaded and the cause is almost always an edematous condition. the glucose is about 300mg/dL high. Sodium is gained. brain disease. think Goodpasteur. where sodium falls 1. So per unit of blood. Urine Na+ < 10. drug side effect. sodium of 131. think acute tubular necrosis (ATN). think pre-renal and give fluids. the patient’s sodium is not truly low thus do not treat the sodium. hyper-proteinemia was ruled out. * Hyponatremia mild or gradual change the patient will most likely be asymptomatic. BUN/Cr > 20x normal. SIADH. there is less sodium even though the concentration has not changed. * Low osmolality with euvolemia. DO NOT DISTRIBUTE . Causes osmotic fluid shift from intracellular space into the blood.2 (normal). thyroid function. * “Real” hyponatremia is lab hyponatremia (from a basic metabolic panel) with low osmolality. accompanied and exceeded by secondary water gain. that glucose accounts for about 3. * With normal osmolality pseudo-hyponatremia. Fluid shifted into blood dilutes Na+ level. in the healthy patient there is a small amount of protein/lipid per block of blood. * First step in determining why a patient is hyponatremic is determining the osmolality. or a simpler but less perfect method is 2*Na + 10). neoplasm-related (most common is small/oat cell in the lung).6 per 100mg/dL increase in glucose. So the glucose does not explain all of the drop in the sodium. with a normal amount of sodium. * Patient presents with diabetes. Normal renal. * Causes of hyponatremia include pseudo-hyponatremia. so 3*1. sweat.8. * SIADH has urine osmolality inappropriately high in the face of hyponatremia with low serum osmolality. lab shows osmolality is low. there are multiple causes including SIADH. So again. symptoms include seizures. so the patient’s volume status. Does the glucose explain the level of hyponatremia? Here. and hepatic failure or cirrhosis. * Pseudo-hyponatremia can occur also with normal osmolality. diuretics. High volume status assessed with edema. multiple causes). treat the glucose. there is less space for the sodium and water component of blood. volume depletion. With severe or rapid change. With moderate change.26 - . urine osm is high/concentrated. * If the ECF is high (hypervolemia). glucocorticoid deficiency. also known as psychogenic polydipsia). usually glucose. * Hyponatremia with high osmolality (hyperglycemia). lab artifact from hyper-trigleridemia or hyperproteinemia (e. kidney. What test will show the cause of the patient’s hyponatremia? Answer is serum lipids (triglycerides). * Low osmolality with hypovolemia. When protein/lipid increase.g. Emergency treatment is hypertonic saline (3% or 5%). and burns. low volume status assessed with tachycardia and orthostatic hypotension. Thus sodium is normal so the glucose explains this pseudo-hyponatremia. the patient has fluid loss with causes including GI. diarrhea. such as in high osmolality of hyperglycemia (1.6mg% sodium per 100mg% glucose). Diagnoses to consider are congestive heart failure. Normal blood osmolality is between 280 and 300. adrenal. sodium is 128. Thus adjusted sodium is 136. So in hyperglycemia. bowel obstruction. Labs show glucose of 402. Renal loss (urine Na+ > 10) due to diuretics. hypoaldosteronism. coma. Not likely to show on the exam but can happen in clinical practice is when a phlebotomist draws blood at the antecubital fossa when D5W is running at a distal hand IV site. the next step is to measure the extracellular fluid volume. Total protein is 7.2 in sodium drop. edematous conditions. There is a magnitude effect. nephrotic syndrome. sweat. so sodium is actually 129 adjusted. Osmolality can be determined by direct measurement (best) or by calculation (osmolality = 2*Na + glucose/18 + BUN/2. So hyper-triglyceridemia is next. and hypothyroidism. Hemoptysis. ADH is secreated causing the patient to retain fluid and excrete concentrated urine.8 difference for sodium. or due to skin loss from burns.
carbamazepine. * Key points about hyponatremia: determine serum osmolality.g. Get a urine osmolality if volume status is normal. and if severe and can’t find a reversible cause then demeclocycline or lithium. If you correct the sodium too rapidly. vinblastine. * Emergency treatment for serious hyponatremia is hypertonic saline. then the problem is in the brain (central DI). like Conn syndrome primary hyperaldosteronism from renal disorder. With severe hypokalemia. lithium. Other causes include licorice in high quantities due to mineralocorticoid effect of glycyrrhetinic acid. stop drug). DO NOT DISTRIBUTE . Meds include furosemide and albuterol. meaning urine output drops and becomes more concentrated. If there is a response to the ADH. digitalis/digoxin toxicity is potentiated. fluoxetine. phenothiazines. Causes include diarrhea with loss of potassium in the stool. vincristine. Sodium is 126. The urine will not change concentration either. or Cushing syndrome from adrenal excess. * Drugs that mimic ADH function include oxytocin. it can cause seizures due to cerebral edema. beta-agonists (e. and chlorpropamide. * What is the most common cause of hypernatremia? Answer is dehydration. there is no change in urine volume because there is no ADH to do it. and non-specific T and U wave changes. give vasopressin in the form of desmopressin (DDAVP) usually intranasal or sometimes subcutaneous or IV.g. the problem is the kidneys (nephrogenic DI). What are the possible causes of hyponatremia? Vomiting could cause dehydration. * Symptoms of hypokalemia if mild are asymptomatic. * Treatment is to reverse the cause if possible (e. How do you determine the cause? You need osmolality level and volume status. furosemide with normal saline (to raise blood sodium). cardiac arrhythmias occur. NSAIDS increase prostaglandin (PG1). glucose 342. * 82yo man presents with 1 week of vomiting and 2 days of confusion. low serum osm. the furosemide with loss of potassium in the urine. vincristine. with low osmolality you need to determine ECF. theophylline. phenothiazines. which impairs urinary concentration ability. * Treatment for dehydration is isotonic fluids with slow correction of sodium (1mEq/2h). and insulin that increases potassium entry into cells. tumor) and nephrogenic causes (lithium. the urine volume will decrease with time and the urine output will be more and more concentrated. albuterol) that increase potassium entry into cells. fix pneumonia. tolbutamide. MAO inhibitors. NSAIDs. Thiazides cause Na+ depletion and water resorption in the kidney. and less commonly in diabetes insipidus (DI) where water loss is up to 20L per day. narcotics.g. The more appropriate term now used is osmotic myelinolysis. burns. At any level of hypokalemia. * Rare causes of hypokalemia include hyperaldosteronism. Fluoxetine and chlorpropamide can cause SIADH. In a normal person. cyclophosphamide. seizures. -------------------------------------------------------------------------------------------------------------------------------------------Electrolyte Disorders: Hypernatremia * Hypernatremia is likely the least common of the sodium and potassium abnormalities. * Treatment of nephrogenic diabetes insipidus is to give thiazides or NSAIDs. cyclophosphamide. Hypothyroid can cause ADH syndrome. or Bartter syndrome from volume depletion secondary to impaired renal resorption of NaCl. * If you think the patient has DI. * Symptoms include lethargy. * Diagnosis of SIADH is accomplished by seeing hyponatremia. * Drugs to pay attention to here include TCAs. * If you cannot correct the sodium. and has pneumonia. * 73yo man with COPD and CHF has had diarrhea for 3 days. Identify three possible causes of hypokalemia. * Causes include fluid loss in excess of Na+ loss commonly occurs in insensible loss from sweat (extreme exercise). and the albuterol with increased cellular resorption of potassium. various renal diseases). and coma. the patient is given ADH. also medication such as diuretics causing renal loss. moderate include muscle weakness. Now has increased SOB (shortness of breath). High glucose could cause pseudo-hyponatremia. muscle cramps. -------------------------------------------------------------------------------------------------------------------------------------------Electrolyte Disorders: Hypokalemia * Hypokalemia common causes are GI loss from diarrhea. high and normal osmolality are artifacts of high glucose/lipids/protein. think about diabetes insipidus. brain tumor).27 - . chlorpropamide. DI can occur due to central causes (idiopathic. clofibrate. tube drainage. * Drugs that increase ADH action include chlorpropamide. Takes thyroxin.Study Notes – Internal Medicine James Lamberg 28Jul2010 *Drugs that increase ADH secretion include TCAs. resulting in quadriplegia. restrict fluids. * Treatment of central diabetes insipidus is to correct the underlying problem if possible (e. carbamazepine. In diabetes insipidus. and commonly occurs in GI loss from diarrhea (e. You also need urine sodium if volume status is low. confusion. Received multiple albuterol treatments in the ED (emergency department). fluoxetine. Then. used in labor induction. * Correcting hyponatremia too quickly can cause central pontine myelinolysis. children). high urine osm. If there is no response to the ADH. do a water restriction test.g.
occurs in acidosis (H+ into cells.42/47/PO2/33/97%. * Metabolic alkalosis is either a loss of H+ or a gain of HCO3. This can also occur if blood is drawn proximal to a running IV drip that contains potassium. Potassium is one of the chemicals used for lethal injection because it causes heart block and asystole. IV replacement maximum is 10mEq/hour via peripheral IV or 20mEq/hour via central line.52/25/PO2/27/99%. acute COPD. She presents for a routine checkup. sudden cardiac conduction defects preceded by classic ECG changes (talk pointed peaked T-waves). * Respiratory alkalosis will have increased pH. RR is 36.4 +/. Movement of potassium from cells into the blood can cause hyperkalemia. pain attack). Could be a patient on birth control pills with acute pulmonary embolism. * 24yo female comes to the ED feeling like she is suffocating. * 67yo woman with HTN is on HCTZ. PCO2 at 25 is low. low sodium. complains of fatigue. Pseudo-hyperkalemia can occur as an artifact from venipuncture or cell lysis from shaking the blood tubes.37 is acidosis and pH > 7. * Arterial blood gas (ABG) gives you pH.6. Hyperventilation lowers PCO2 and breath holding or shallow respirations will increase PCO2. You get PCO2 (normal 35-45) and should determine respiratory rate/volume. * Metabolic alkalosis is a chronic process. never overcompensation. which can vary by the altitude you live at. You get HCO3 (normal 20-28). decreased PCO2. early aspirin toxicity. Patients needs treatment if ECG changes present. This is uncommon except in conjunction with certain medications (e. An excessive rate causes cardiac conduction defects including heart block and/or asystole. -------------------------------------------------------------------------------------------------------------------------------------------Acid-Base Disorders * A normal blood pH is 7. HCO3 rises with time to compensate almost back to a normal pH. leading to falsely high potassium levels. -------------------------------------------------------------------------------------------------------------------------------------------Electrolyte Disorders: Hyperkalemia * Causes include increased potassium intake. these changes are rapid. could be renal failure. Give CaCl or Ca++ gluconate infusion.g. The PCO2 being high is respiratory compensation. This is done with glucose and insulin. respiratory rate slows to raise PCO2 thereby increasing pH almost back to a normal value. likely due to the hyperventilation. Labs reveal creatinine increased to 4. rhabdomyolysis. low chloride. * What if the patient above had an O2 sat of 76%? This is not acute anxiety or panic attack. So PCO2 of 47 is high. where you can determine if this is acidosis or alkalosis.43 is alkalosis. pneumonia). and HCO3 of 33 is high. * 67yo woman with diabetes and hypertension is on glyburide and ACE inhibitor. potassium sparing diuretics. and if sustained the kidneys will retain HCO3 in an attempt to lessen the acidosis. ACE-inhibitors). This is respiratory alkalosis. * Respiratory alkalosis is caused by hyperventilation.03. increased PCO2. and sleep apnea. ABG is 7. This is metabolic alkalosis defined by high pH and high HCO3. This is a lung problem. an inability to blow off CO2. * Respiratory acidosis caused by hypoventilation (acute or chronic). HCO3 unchanged because not enough time. Chronic causes include COPD. Another causes is deceased renal excretion from renal failure or medications like spironolactone and ACE-Is. K+ out). with bicarbonate working as a metabolic buffer. Electrolytes show low potassium. should be above 90% normally. increased HCO3. replace orally. Common causes of HCO3 gain include NaBicarb ingestion (multiple antacid pills) and milk-alkali syndrome (CaCO3). Last step is to get rid of the potassium from the body. such as an error in the hospital with excessive potassium administration. HCO3 unchanged because not enough time. A pH < 7. also with bicarbonate as the alkalosis drives potassium into cells.5 and potassium is 6. Whenever possible. Next step is to lower the potassium level by driving potassium into the cells. She appears anxious. these changes are slower (2-5 days). Why did her potassium become high? There are a number of reasons include the ACE-I. obesity. * Symptoms include weakness that increases with potassium level. This is done with cation-exchange resin (kayexalate) or dialysis if renal failure. Hemolysis of cells causes the potassium to be released from the cells. with compensatory slowing of respiratory rate and increase in PCO2. O2 sat typically in mid-90s. Drives down the PCO2 with no time for metabolic compensation.Study Notes – Internal Medicine James Lamberg 28Jul2010 * Treatment of hypokalemia is done by replacing potassium. They still have potassium in their body but it is no longer in the circulation where it would induce cardiac arrhythmia. or asthma. DO NOT DISTRIBUTE .28 - . Either way it is a lung problem. Pickwickian (obesity hypoventilation syndrome). ABG also gives O2 and PO2. Acute causes include narcotics.interchange). Exam shows orthostatic hypotension. * Respiratory acidosis has decreased pH. anxiety (acute pain. has tightness in her throat and chest.0. ABG shows 7. acute pulmonary disorder (pulmonary embolism. and rarely familial periodic paralysis. * Metabolic alkalosis has increased pH. Common causes of H+ loss include prolonged vomiting or other GI loss and diuretics (H+ and Cl. Hypoaldosteronism and adrenal insufficiency are other cause. How will you treat this? * Treatment should start with protection of the heart.
inability to excrete acid. hematologic malignancies). amphotericin B. Common causes are diarrhea and renal tubular acidosis (RTA). lactic acidosis. Diagnosed by giving acid load/challenge test and still can’t acidify urine. Nevada). metastatic cancer). with causes including addition of acid. Lactic acidosis is due to overproduction of lactic acid.3. urate about 5%. Treatment is oral bicarbonate. salicylate. ABG shows 7. This is a narcotic overdose with respiratory acidosis due to hypoventilation. and increased respiratory rate as compensation in an effort to blow off PCO2 thereby increased pH almost back to normal. Occurs with aldosterone or adrenal insufficiency and diabetes. This is metabolic acidosis as bicarb is low. ABG shows 7. calcium phosphate. What is the most likely cause of the this patient’s normal anion gap metabolic acidosis? Most likely diarrhea. has altered mental status. What would be the best test to distinguish diarrhea from RTA? Answer is urine pH. Wilson disease. klebsiella. * MUDPILES: methanol. lithium.3).37/5/PO2/34/90%. Intoxication causes addition of non-HCl acids. urine would be inappropriately high pH in RTA. ethylene glycol. are radiolucent and may not be seen by CT or other x-ray. Diagnosed by seeing bicarbonate lost in urine in the face of acidic blood.g. Her PCO2 is high. so normal anion gap (11 +/.37 is not alkalosis. Arizona. diabetic. magnesium/ammonium/phosphate (“triple phosphate” or struvite). * Oxalate. Diagnosed by high urine sodium with salt restriction (salt restriction test). * Type 2 RTA occurs in the proximal tubules of the kidney. Is this metabolic or respiratory? Answer is metabolic acidosis. * 17yo with diabetes has not been taking his insulin. vitamin C excess. lactic acidosis. * High anion gap acidosis is an excess of non-HCl acid.29 - . occurs rapidly. Comes to the ED because she is becoming gradually SOB. fludrocortisone. vitamin D intoxication).31/30/PO2/17. renal failure (uremia). HCO3 18. * Main causes of calcium oxalate/phosphate stones include increased calcium absorption (sarcoid. * Renal tubular acidosis key clue is the inability to acidify urine. Anion gap is normally 11 +/.g. iron/INH. either high-anion gap (anion gap) or normal anion gap (nonanion gap). struvite about 5-10%. K 2. the body does not overcompensate. ABG shows 7. Seen in myeloma. ABG shows 7.” There are four major causes: ketoacidosis (alcoholic. which should be acidic (< 5. Inability to absorb bicarbonate until levels very low. * Main causes of uric acid stones include gout. PCO2 being low is compensatory. As compensation. Fanconi syndrome. How do we know this is not primary metabolic alkalosis (i. vitamin D deficiency. Treatment is volume restriction.9. * 72yo man has 4 days of diarrhea and presents to ED with weakness. Inability to acidify urine. or intoxication (ethylene glycol. * Metabolic acidosis is a relative increase in the quantity of acid. pseudomonas). Could be RTA. others). idiopathic hypercalciuria. * Metabolic acidosis is the most complicated of the group. tissue breakdown (e. salicyclates.29/29/PO2/17/97%. * Five kinds of stones: calcium oxalate (most common). inc HCO3 with inc PCO2 compensating)? We know this because the pH of 7. paraldehyde/phenformin. hyperoxaluria (fat malabsorption as fat binds to calcium. * Must determine which type of metabolic acidosis. Normal anion gap acidosis is excess HCl or loss of HCO3. urinary pH typically > 5. Presents with hyperkalemia. Cl 113. phosphate about 10%. * Main causes of struvite stones include infection with urea-splitting bacteria (proteus most common. so 8-14. leaving oxalate for excessive absorption). Respiratory rate is 7.4) in the presence of blood acidemia. Renal failure causes inability to excrete organic (non-HCl) acids. * Ketoacidosis is due to overproduction of ketone bodies. Pupils small. Urate may not be seen on plain x-ray. * Anion gap > 14 caused by overproduction or under-excretion of an acid other than HCl. and loss of base (HCO3). uric acid.Study Notes – Internal Medicine James Lamberg 28Jul2010 * 27yo man found unconscious on the street. * 72yo woman has COPD worsening over weeks. starvation). diabetic ketoacidosis. Anion gap = (Na + K) – (Cl + HCO3).4 or even overtly alkaline. * Type 1 RTA occurs in distal tubules of the kidney. DO NOT DISTRIBUTE . sickle cell. Needle tracks on arms. What is the anion gap? Gap is 12. hyperparathyroidism. uremia. Lytes are Na 140. and struvite have calcium and are radio-opaque. body is breathing fast to bring down PCO2. Seen in kidney stones. * Oxalate stones account for about 70%.28/56/PO2/28/84%. Chloride levels are unaffected “normochloremic. -------------------------------------------------------------------------------------------------------------------------------------------Kidney Stones (Nephrolithiasis) * Urolithiasis occurs in 1-5% of the US population. destructive bone disease (myeloma. so likely a CO2 retainer with the COPD. more common in desert southwest (e. cysteine (rare). cysteine rare. Treatment is mineralocorticoid replacement.e. * Metabolic acidosis has decreased pH. * Anion gap < 14 (normal) usually caused by HCO3 loss in GI tract or urine or inability to excrete acid in urine. alkaline urine favors crystallization of struvite and can result in large stones (staghorn calculi). decreased HCO3. * Type 4 RTA occurs due to hypoaldosteronism. methanol wood alcohol. phosphate. Is this acidosis or alkalosis? Answer is acidosis.
destructive bone disease (serum Ca level). do spiral CT.5cm) and ureteral (<1. vitamin C excess (discontinue vitamin C). no longer test of choice. Small stones at the ureteropelvic junction (UPJ) almost always pass. or what is the best test to confirm diagnosis? Answer is non-contract helical (spiral) CT scan. * Initial tests in a “stone workup” include looking for increased calcium absorption (24h urine calcium). control hypertension.g. * Say the 26yo female is not pregnant and the spiral CT shows a small radiolucent stone in the ureter. ovaries. Mitral valve prolapse (25%). impaired circulation due to distortion of renal vasculature leads to increased renin-angiotensin. treat UTIs/stones. * For small stones (<5mm) in lower ureter is observation. Answer is urinalysis for hematuria. * You should always try to determine the type of stone the patient has. * Extra-renal manifestation of PKD include hepatic cysts (50%). Cause is uncertain. * 35yo male has sudden onset of severe flank pain radiating to groin. * Spiral CT is the test of choice as it is fast. difficult to interpret as gas may be in the way. vitamin C excess (history). bladder x-ray) is useful for patients with known stone disease. * For complex stones (e. identifies radio-opaque and even some radiolucent stones. The absence of hematuria argues strongly against kidney stone. hematuria. pain may be constant or spasmodic. asymptomatic in childhood. Can be single or multiple. complex cysts (rule out cancer).Study Notes – Internal Medicine James Lamberg 28Jul2010 * Kidney stones present with severe flank pain radiating to the groin. No treatment is needed unless large or symptomatic. idiopathic hypercalciuria (24h urine calcium). It can be combined with lithotripsy. What is the best test to make a diagnosis? Answer is renal ultrasound to rule out PKD. What is the most appropriate initial treatment? Answer is analgesics (e.5cm) stones. 10% are sporadic mutations without family history. * Percutaneous nephrostomy is used for obstructed stones to drain the kidney via a tube and prevent backflow. Pain medication may be one of the first priorities. Large or with significant obstruction requires surgical intervention. To do this you strain the urine and send for urinalysis. dialysis/transplant for ESRD. fat malabsorption (history. * 32yo man is seen for hypertension and hematuria. infections. destructive bone disease (treat problem). fat malabsorption (treat problem).30 - . What is the next step in determining diagnosis. Tells you that father and cousins had a similar problem and both died of hypertension-related renal failure. Is a homogenous cysts without echos (fluid filled sac). with nausea and vomiting. idiopathic hypercalciuria (thiazides). pain onset often sudden. ureter. Creatinine is 1. hyperparathyroidism (treat problem). morphine) and high flow IVF. Colon diverticula more often than in general population. only 2/3 have cysts in their teens. infancy). For adults and children at risk. If negative. struvite) or extensive anatomic abnormalities. cysts not universally present until about 30s. * PKD manifests with hypertension in the kidneys.5. then do sonogram. Sonogram is the test of choice for identifying stones in pregnant women. * Ureteroscopy involves putting cystoscope through urethra up into bladder then fragments stones and pulls them out with forceps or baskets. simple cysts (incidental). half have ESRD by age 60. * Genetic diagnosis can be done with prenatal amniocentesis and chorionic villus sampling (CVS). What is the next step in the diagnostic evaluation? Answer is pregnancy test. stones. bowel prep needed for good pictures. hyperparathyroidism (serum Ca level. diagnose symptomatic patients. Intracranial aneurysms (10%) berry aneurysms that can lead to subarachnoid hemorrhage. If pregnancy test is positive. * PKD causes 5-10% of end stage renal disease needing dialysis. What is the best first test to support the diagnosis of kidney stone. * Simple renal cysts are usually incidental findings on sonogram or CT. high blood pressure via RAAS. * Lithotripsy (ESWL) can be used for small renal (<2. most sensitive. nausea and vomiting common. * PKD is autosomal dominant in 90% of cases. usually single. -------------------------------------------------------------------------------------------------------------------------------------------Renal Cysts * Three types of cystic kidney disorders: polycystic kidney disease (PKD) in autosomal dominant form (1:300 to 1:1000) and autosomal recessive form (rare. * PKD involves multiple renal cysts. Urinalysis shows hematuria. * PKD diagnosed with renal ultrasound.g. IVP (intravenous pyelogram) requires contrast. with nausea and vomiting. also pancreas. DO NOT DISTRIBUTE . spleen cysts. greasy stools). gene linkage studies are useful if considering kidney donation to affected relative. KUB (kidneys. symptoms develop in 20s and 30s including pain from kidney size pushing on renal capsule. PTH level). * Treatment of PKD is manage complications. screening of relatives at risk. * Treatment for increased calcium absorption (thiazides). * 26yo female presents with sudden onset of severe flank pain radiating to groin. So the patient will urinate at home into a funnel until a stone or particles are found. Stones and infection also occur. open surgical removal is performed. Renal failure occurs with progressive decline in function.
Also nitroglycerine (with MI). and basic labs. aortic regurgitation is echocardiogram. creatinine. regardless of size. when do you have to get the patient back for a confirmation? If BP systolic > 180 or diastolic > 110. aldosteronism is DO NOT DISTRIBUTE . * Most common presentation is incidental finding in an asymptomatic individual. * Ambulatory BP monitoring gives data for a 24h period. Cushing is dexamethasone suppression test and/or cortisol. Cushing is remove pituitary adenoma. * Chronic complications include CVA (400. confirm on 2 subsequent visits. < 5% of HTN is secondary. then yearly. obese.000 ESRD/year). * Complex renal cysts vary in size. blurred vision). * After you get a first blood pressure reading. eye disease. a complex cyst is cancer until proven otherwise. Aortic regurgitation has high systolic pressure and low diastolic pressure. murmur. * Hypertensive emergencies need immediate treatment: angina or CHF. * 32yo previously normotensive man sees you for a work physical. Pheochromocytoma presents with sympathetic episodes. * What is the initial treatment if a secondary cause is suspected? Medication-induced is stop meds and follow BP. cerebral impairment (ischemia. Hypertensive emergency is uncommon. Polycystic kidneys can be found by mass or hematuria. * Say the patient comes back and their HTN is confirmed. average of 2 readings. renal failure is BUN/Cr. papilledema. Cushing disease will have striae. * Stage 3 hypertension is systolic 180+ or diastolic 110+. due to some other condition that is often reversible. subarachnoid hemorrhage. do history. and seek/control atherosclerotic (ASHD) risks. then 1 month. buffalo hump. enalapril. His history and exam are otherwise unremarkable. renal artery stenosis is captopril renogram in young (fibromuscular) and Doppler flow in elderly (atherosclerotic). then 2 months. * “White-coat” hypertension is thought to occur in about 20% of cases of diagnosed HTN. polycystic kidney is ACE-I (maybe) and renal transplant. seasonal rhinitis spray). rounded moon-facies.31 - . and males > females. that is 1/4 of the adult population. seated with arm at heart level. Chronic complications can develop. * Hi-normal is systolic 130-139 or diastolic 85-89. pulse striking earlier in radial than femoral arteries. By definition. * Investigating secondary causes can be done by history. complex renal cysts are cancer until proven otherwise and need CT-guided needle biopsy. exam. Renal artery stenosis is found by bruit on abdominal exam or sudden abrupt onset of HTN. patient may present with heart attack or retinal hemorrhage. coarctation is surgical. Renal failure can be discovered by creatinine level elevation. What is the next step in the evaluation. multiple (complex) echos/septations seen on CT or ultrasound. or found during workup of hematuria or abdominal pain. What is the next step in evaluating his blood pressure? Answer is return in 1-2 months. severe headache). Sonogram to study gallbladder reveals gallstones. CT scan confirms findings. Hyperaldosteronism will come with low potassium. * Stage 2 hypertension is systolic 160-179 or diastolic 100-109.g. Hyperthyroidism can cause HTN (tremor. potassium. * Chronic complications include heart disease with >1million MIs per year. Medication causes include birth control pills and alpha-agonists (e. 60% of persons over age 65 have HTN and 75% are not controlled. coarctation is ultrasound studies. then 1 week. pheochromocytoma is VMA and metanephrines and catecholamines. 400. If BP systolic 130-139 or diastolic 85-89. renal artery stenosis is angioplasty. * Stage 1 hypertension is systolic 140-159 or diastolic 90-99. Patient has no symptoms from left kidney. physical. hyperthyroid is ultra-sensitive TSH. polycystic kidney is renal sonogram.000 strokes/year). but also a small (2cm) cyst on left kidney with complex echos. hyperthyroid is beta-blockers and anti-thyroids. Answer is cyst aspiration/puncture. renal failure (5.Study Notes – Internal Medicine James Lamberg 28Jul2010 * Complex renal cysts are usually incidental findings on sonogram or CT. BP is 170/99. goiter). * Epidemiology shows 50million Americans with HTN. If BP systolic 160-179 or diastolic 100-109. seek end-organ damage. * 62yo man is being evaluated for RUQ abdominal pain. * BP measurement method: patient resting quietly for 5 minutes. Normal is systolic < 130 and diastolic < 85. labetalol. diabetics. If BP systolic 140-159 or diastolic 90-99. * High risk groups for HTN include African Americans. Must do a percutaneous aspiration biopsy (CT needle aspiration). * What is the best test if a secondary cause is suspected? Medication-induced is stop meds and follow BP. and no hematuria. If BP systolic < 130 or diastolic < 85. then every other year. bladder encircles 80% or more of arm. * Treatment for hypertensive emergency is nitroprusside infusion. * Essential hypertension has no clearly identified cause or reversible process. useful for suspected “white coat” hypertension.000 new CHF per year. Perform a physical exam and laboratory investigations to seek secondary causes. -------------------------------------------------------------------------------------------------------------------------------------------Hypertension (HTN) & Hypertensive Emergencies * Optimal is systolic < 120 and diastolic < 80. * So for secondary HTN causes. * Again. aldosteronism is aldosterone level. acute eye findings (hemorrhages. Coarctation of the aorta can be found by pulse lag.
mild renal insufficiency. Vancomycin not superior in efficacy to ox/clox/diclox/naf. just superior in its resistance pattern. renal failure is renal transplant. Macrolides with clindamycin will cover staph/strep. sedentary lifestyle. usually in elderly. cloxacillin. * Antibiotics for staphylococcus and streptococcus are oxacillin. SVT. then we should avoid all the beta-lactam antibiotics. 5% cross-reaction with penicillins at most and almost never anaphylaxis. * What if patient says they have a penicillin allergy. * Macrolides: erythromycin. * Another alternative for staphylococcus and streptococcus (e. and laryngeal edema so they had to get intubated. smoking cessation. cephadroxil. patient may be confused about treatment regimen. CHF. pheochromocytoma is alpha-blockade and surgery. What is the most appropriate test for a secondary cause of hypertension? Answer is renal ultrasound to rule out polycystic kidney. * With methicillin-sensitive staphylococcus. AAA (exam vs sono). is artery calcification that prevents full compression of the artery by the blood pressure cuff. you will find there was beta-lactamase in the staphylococcus. gram negative rods. * Hypertension in pregnancy. and stridor. firstgeneration cephalosporins like cephalexin. that causes a little rash. thus giving a falsely high reading. C-reactive protein level also not proven to be linked to heart disease. DO NOT DISTRIBUTE . * Medications are first-line for uncomplicated essential hypertension (stage 3. ACE-I will improve renal blood flow a bit and lower risk of progressive renal damage. obesity. most stage 2. homocysteine levels). Use ox. azithromycin. * Hypertension treatment initially for stage 1 and maybe stage 2 is lifestyle modification: weight reduction. carotid bruits. newer risk factors (C-reactive protein. * So what antibiotics go along with staph/strep. naf. * 45yo previously normotensive man sees you for work physical and BP 165/92. History is unremarkable except vague LUQ abdominal pain for past 6 months. lower extremity pulses. Alpha blocker for prostatic hypertrophy. Other labs are normal including creatinine. * Special circumstances: ACE-I used in diabetes. possibly alcohol reduction is in large amounts. hyperlipidemia. most common cause of osteomyelitis is S. * 45yo previously normotensive man sees you for work physical and BP is 170/99. -------------------------------------------------------------------------------------------------------------------------------------------Kaplan Videos (2001) – Infectious Disease with Dr. diabetes. dicloxacillin. MD -------------------------------------------------------------------------------------------------------------------------------------------The organisms that cause certain diseases do not change over the years. nafcillin (not methicillin). * Calcium-channel blocker used in isolated systolic hypertension in elderly. cefazolin. For lifethreatening penicillin allergies.32 - . penicillin. Most common cause is noncompliance. Vancomycin works. what do you use? Not methicillin. but are not first choice. exam shows LUQ fullness. Why don’t we use methicillin? Because it causes interstitial nephritis. teratogenic. -------------------------------------------------------------------------------------------------------------------------------------------Overview of Antibiotic Therapy * Most common cause of pyelonephritis is E. aureus. possibly better than beta-blockers in African American population if adding to diuretic.g. clox. then got IV steroids. stage 1 if it does not respond to lifestyle modification). but not for staphylococcus. Diuretics (thiazides) are first or beta-blockers. * Homocysteine levels can be lowered with vitamin B6. * Risk factors for atherosclerotic heart disease (ASHD) are smoking. salt reduction. otherwise no ASHD risk factors. * End-organ damage can be investigated by looking for retinopathy. Labetalol or hydralazine also acceptable. amoxicillin alone is good for streptococcus. and hypotension. Contraindicated drugs include ACE-I and angiotensin receptor blockers (ARBs). clarithromycin.Study Notes – Internal Medicine James Lamberg 28Jul2010 remove aldosterone tumor. ECG (vs echo vs nothing) for left ventricular hypertrophy. or recent MI. Consider alcohol abuse and NSAIDs. Conrad Fischer. * Ampicillin. Beta-blocker for migraine headache. Clue to this palpable artery with inflated cuff. Multiple BP readings over 2-3 months confirm hypertension. * What if you start treating a patient and the hypertension is not responding. penicillin allergy) is a beta-lactam drug. but being investigated. History reveals 1PPD smoker for 30 years. diclox. vitamin B12. What is the best initial step in his treatment? Answer is smoking cessation. so don’t worry if the allergy is a little rash. and anaerobes? * If you do PCR resting on Egyptian mummies from 5 thousand years ago. folic acid. CHF due to systolic dysfunction. * “Double-duty situations”: calcium-channel blocker for Raynaud. Multiple BP readings over 2-3 months confirm hypertension. exercise. then dopamine drip in the ICU. atrial fibrillation. Urinalysis shows hematuria. but should be reserved for methicillin-resistant staph aureus (MRSA). aortic regurgitation is ACE-I and valve replacement. * Osler phenomenon. no evidence it improves heart disease. Re-consider secondary causes. recommended drugs: methyldopa is first line. choice for life-threatening penicillin allergy. Physical exam and all lab tests are unremarkable. The antibiotics do however. coli.
So what will tell you right now what type of organism you have? Answer is cell count. it causes aplastic anemia and Gray Baby Syndrome. Lyme also not seen on Gram stain because it is a spirochete. * So 57yo man has fever. no other use. stiff neck. aminoglycosides (gentamycin. tobramycin. If you see 1000s of polys. ceftriaxone). and focal findings. * CSF cell count: Only bacterial gives you 1000s of polys.33 - . * Cephalosporins range from strong Gram-positive coverage at first-generation (poor Gram-negative) to strong Gram-negative coverage at third-generation (poor Gram-positive). * Rocky Mountain Spotted Fever (RMSF) is not seen on Gram stain because it is intracellular (rickettsia). enterobacter. then follow up with fluconazole forever. Gram stain negative. Doxycycline used for Lyme (mild disease: rash. You also can’t see TB. Other information from the LP can help tell you the diagnosis. Rocky Mountain Spotted Fever. syphilis. * So. * Nitrofurantoin used for UTI in pregnancy. don’t jump to imipenem. positive in 95-98%. rickettsia. streptomycin. altered mental status (confusion. second-generation cephalosporins (will not cover pseudomonas). encephalopathy). coli. carbapenems (imipenem. Fourth-generation cephalosporins (cefepime) are a combination of first-generation and third-generation. * Antibiotics for Gram-negative rods are aztreonam. pseudomonas. What if they want you to know it’s a brain abscess? Fever. as these are intracellular organisms. you should start the patient on antibiotics first (dose of ceftriaxone). clindamycin (does not cover bowel well). give ceftriaxone. Chlamydia.” * TMP-SMX is only good for uncomplicated cystitis and prophylaxis against pneumocystis pneumonia. * Tetracycline is not the correct choice anymore. Now what? Answer is serologic testing to look for specific antibody against Lyme and RMSF. What about 10-100s of lymphocytes? Could be fungal (cryptococcus). expect HIV patient with < 50 CD4 T-cell count. Remember the Weil-Felix test? Forget it. use doxycycline instead. fluoroquinolones (ciprofloxacin. A specific additional symptom to lead you down the right path would be stiff neck (nuchal rigidity). viral meningitis. When do you wait for results of the culture? Never. Legionella. Which gives it most often? Bacterial. right? We just get some IgM acutely and IgG chronically. azlocillin. meropenem). Doesn’t that ruin the sensitivity of the LP culture? Yes. but you’d rather be alive with a clean LP than dead with an accurate LP. implying meningitis. If you have an exclusively anaerobic infection. CSF from lumbar puncture shows 10-100s of lymphocytes. India Ink is about 50% sensitivity (good if positive. culture negative. * For cryptococcus meningitis. * If you are going to do a CT prior to the LP. moxifloxacin). Gram-stain is 50-60% sensitive. or syphilis on Gram stain. All other tests are compared to culture. mezlocillin). Best initial test? Answer is not India Ink. Should you start this patient with fluconazole? No. what is the most accurate diagnostic test? Answer is culture. * Carbapenems cover Gram-negative and Gram-positive. so they cover Gram-positives and Gram-negatives. Only do a CT scan prior to a spinal tap if papilledema or focal findings that would imply a brain mass/abscess. such as “squeeze my hands. klebsiella. strep pneumonia. so won’t be positive most of the time.Study Notes – Internal Medicine James Lamberg 28Jul2010 * Gram negative rods include E. neomycin. use amphotericin B. headache. levofloxacin. ticarcillin.” because you cannot determine focality. -------------------------------------------------------------------------------------------------------------------------------------------Meningitis * 57yo man comes to the ED with fever and a headache. tuberculosis. sparfloxacin. If you had a mass lesion that was so small it did not cause focality. What is the first test? Do you do a lumbar puncture or a CT scan? What is the first test? Lumbar puncture (LP). Patient also needs to be able to follow commands. very sensitive and specific. * With papilledema you worry about herniation. This helps you determine if you should use doxycycline or ceftriaxone. Amphotericin B (better than fluconazole for saving life in meningitis). but you should not use them for Gram-positive infections (like strep throat) because there are better drugs exclusively for Gram-positives.’” * When you have infectious diseases. proteus. amikacin). facial nerve palsy). it can happen within hours. an LP would not cause herniation. Lyme disease. DO NOT DISTRIBUTE . “Do not swat a fly on your friend’s head with a hammer. * Chloramphenicol is never the right answer. headache. headache. citrobacter. “You go to do a rectal later and say ‘my that’s a smooth prostate’ and the patient says. viral. else cryptococcal meningitis recurs. carbapenems as well. that’s my pons. * The most common neurologic problem after meningitis is deftness. CN VIII damage. ‘that’s not my prostate. third-generation cephalosporins (ceftazidime. gatifloxacin. However. Photophobia or seizures or nausea or vomiting are too nonspecific here. trovafloxacin. extended spectrum penicillins (piperacillin. where others give 10-100s of lymphocytes. means nothing if negative). Fluconazole is continued life-long. Answer is cryptococcal antigen testing. * Antibiotics for anaerobes are metronidazole (particularly good for abdominal). What about encephalitis? Fever. So this is very easy. * CSF analysis: Which form of meningitis can give an elevated protein and decreased glucose in the LP? Answer is all.
Intrathecal antibiotics is like intra-cardiac epinephrine. If the CT scan is the same. based on American Society of Otolaryngology. How do you know it is not a subarachnoid hemorrhage? There will also be increased WBCs from infection. the only way to know what it is. Congo Crimean fever. You may see a red bulging tympanic membrane. The head CT will most likely be normal. cefaclor would work. Do a CT to see ring-enhancing lesion. You have to suspect the specific disease. Gram stain negative. Answer for management is give ceftriaxone and ampicillin. New York. Two groups of diseases that give ring-enhancing lesions are cancers and infections.” Or you radiate the patient for 6 weeks and they say. leukemia/lymphoma elderly or neonate then do empiric coverage. What is the next step? Head CT. cefuroxime. which has largely replaced the biopsy. target rash (erythema migrans) and outdoor activity. eastern equine encephalitis. Some mild benefit possibly with steroids given prior to starting antibiotics and LP. Colorado tick fever. has a lumbar puncture with elevated protein and decreased glucose. cefixime. TB culture. Next step is not lumbar puncture because the patient will herniate and die. Bolivian hemorrhagic fever. * Test TB (meningitis and pulmonary) with TB stain. * Elderly neonate is HIV positive. If Lyme. So what organism do we have to cover? Answer is listeria. strep. there is no treatment. Massachusetts. “doc. I heard antibiotics don’t work well for glioblastoma. INH. This patient is immunocompromised. If TB.34 - . look for the centripetal rash.Study Notes – Internal Medicine James Lamberg 28Jul2010 * So are with “atypical” results (Gram stain negative.” You have to biopsy to know. Head CT will show ring. -------------------------------------------------------------------------------------------------------------------------------------------Otitis Media & Sinusitis * What is the most sensitive physical finding for otitis media? Answer is immobile tympanic membrane on insufflation. What is suggestive of herpes on a lumbar puncture? Answer is increased red cells. If viral.e. Kentucky. In HIV. Amoxicillin/clavulanic acid works too. oligodendroglioma. AFB (acid-fast bacillus) stain and culture. assume toxoplasmosis and give pyrimethamine and sulfadiazine for a couple of weeks and repeat CT scan. “doc. * Treatment of herpes encephalitis is acyclovir. clarithromycin work. neutrophil and T-cell defects. half the time the otitis media resolves on its own because they are viruses. * Treatment is amoxicillin. do a biopsy to see what is at the ring-enhancing site. not necessary. syphilis serology with a VDRL and FTA on all of them? Nope. astrocytoma. we have a lesion with mass effect giving focal findings. they still are not as common as herpes encephalitis. Tennessee. Methotrexate is given intrathecal in ALL (acute lymphoblastic leukemia). * If you add all those cause of encephalitis and multiply by ten. New Jersey (North East). mildly hemorrhagic. * So again. * When do you answer intrathecal antibiotics? Answer is never. culture negative). -------------------------------------------------------------------------------------------------------------------------------------------Encephalitis * Fever. 90% of the time it is toxoplasmosis or lymphoma.or contrastenhancing lesions. diagnosis is by exclusion of the others. on steroids for CLL. moxifloxacin. western equine encephalitis. centripetal (moves centrally) rash and outdoor activity. your best bet is to answer herpes. plus clear CT scan favors against subarachnoid. headache. * If RMSF. headache. gatifloxacin work as they cover strep pneumonia. Do not do LP. Next step is CT scan (or MRI). ethambutol. Next step is brain biopsy. * Next step depends on HIV status. * If patient is HIV negative. cryptococcal antigen testing. Lyme in Connecticut. anaerobes. and confusion (encephalopathy). HIV (T-cell defect). * When do you answer steroids for meningitis in adults? Answer is TB meningitis. DO NOT DISTRIBUTE . much broader range of disease. If not child. pyrazinamide. toxoplasmosis. RMSF in Alabama. If patient is HIV positive. are we just going to order Lyme. Carolina. and focal findings. because listeria is resistant to all forms of cephalosporins. glioblastoma. Then do a biopsy. Venezuelan hemorrhagic fever. new fluoroquinolones like levofloxacin. it shouldn’t matter. What is the next best step in the management of this patient? Do we give amphotericin or ceftriaxone? HIV is a risk factor for fungal meningitis. Macrolides azithromycin. * Things that put you are risk for listeria include immunocompromised. occasionally fever. rifampin. -------------------------------------------------------------------------------------------------------------------------------------------Brain Abscess * Fever. viral encephalitis. viral serologic testing. RMSF. 3200 polys. Staph. steroids (neutrophil and T-cell defect). This isn’t fungal because there are polys present. resistance) the efficacy of amoxicillin is just as good as any of the other antibiotics. Lots of encephalitis in the world. the radiation isn’t working for my staph aureus. * Second and third generation cephalosporins. diagnose with TB stain and AFB cultures. * Lumbar puncture should come with PCR. if you haven’t recently been treated (i. You don’t want to start antibiotics and have the patient come back with a permanent deficit saying. If the case is clearly encephalitis and they ask diagnosis. nifty idea but not necessary. pain on pulling pinna.
In smokers and COPD patients with lobar pneumonia. chlamydia. you increased your risk of aspiration. pneumocystis pneumonia. consolidations). Get culture and start antibiotics. intoxicated. so we need clue cells to see when there is too much. * What is the most accurate diagnostic test for this sinusitis patient? Answer is culture. You can’t say this is influenza. * Mycoplasma pneumonia usually seen in young. A CT is more accurate than an x-ray. diarrhea. clarithromycin. Answer is give amoxicillin. Answer for treatment is oral penicillin. * Intubation aspiration. loss of gag reflex. moxifloxacin. * What is the best diagnostic test? Answer is biopsy/aspiration. klebsiella. tooth pain. Look for a patient with GI and CNS problems.35 - . -------------------------------------------------------------------------------------------------------------------------------------------Pharyngitis * Symptoms are sore throat. rhinorrhea. * How do we know if the patient has an abscess? Halitosis due to anaerobes. healthy. * Erythromycin has an advantage over the others as it can prevent rheumatic fever. azithromycin. Pen VK. Doxycycline also works. gatifloxacin. Cold agglutinin testing for mycoplasma is not sensitive or specific enough. so not a good way to make a diagnosis. * The rapid strep tests are latex agglutination tests. most common is strep pneumonia. H. sinus tenderness. * Why don’t we Gram stain the vagina? Gardnerella is normal flora. you will not see the diagnosis. adenopathy. * When do you wait for the results of culture? Answer is never. it doesn’t seem logical unless you understand the test.Study Notes – Internal Medicine James Lamberg 28Jul2010 * 28yo female with headache. clarithromycin. then this is bronchitis. looking for the surface antigens of strep pyogenes. * Patient has bilateral interstitial infiltrates. If CXR is normal (no infiltrates. Why do you not do a Gram stain for pharyngitis? It will not tell you if you have strep pyogenes. -------------------------------------------------------------------------------------------------------------------------------------------Bronchitis & Pneumonia * Fever. * How will you know who to do a legionella urinary antigen test for? Not a person exposed to air conditioning or a person exposed to water. Clarithromycin) or quinolone. * If patient is allergic to penicillin. gatifloxacin. 30% h.” Mycoplasma not seen on Gram stain (no cell wall) and not grown in regular culture. * Treatment for mycoplasma or legionella is macrolide (Erythromycin. What test should you order first? Answer is x-ray. * Pseudomonas pneumonia seen in the ICU in intubated patients. * Why is sputum stain not first? Even when you do the culture. abdominal pain. Klebsiella pneumonia is more likely to be seen in alcoholics (but not most common). We do Gram stain the cervix to look for neisseria gonorrhea. It accounts for about 5-10% of community acquired pneumonia. azithromycin. viral pneumonia. All you know is this is a respiratory infection. with or without sputum. We Gram stain sputum because strep pneumonia with lancet-shaped diplococci are not normal flora in the mouth. pneumonia. Test for legionella pneumonia (diagnosis) is urine antigen. * Lobar infiltrates is regular bacterial pneumonia. * Acute otitis media (AOM) is about 40% strep pneumonia. 20% moraxella catarrhalis. staph. Ampicillin would work also. cough. what do we use for pharyngitis? Second or third generation cephalosporins. Azithromycin. * The best initial diagnostic test is an x-ray. bronchitis. If bilateral interstitial infiltrates. hospital acquired infection. could be mycoplasma. patient. What is the next step in management. influenza. moxifloxacin. Most accurate test is Gram stain. but not first. it can’t tell you what type of strep is there. poor dentition. Urinary antigen for legionella is 99% sensitive and specific. * Young healthy person admitted for lobar pneumonia is pneumococcus. Many people will not think about ordering this type of test unless they know it exists. first for respiratory infections. * How do we determine the types of pneumonia if infiltrates are found on CXR? There will be lobar infiltrates or bilateral interstitial infiltrates. legionella. * Why don’t we Gram stain or culture sputum for an abscess? Everyone has anaerobes in their sputum. Atypical means it is not seen on a Gram stain and not grown in regular culture. you don’t get the diagnosis half the time. most common is strep pneumonia. influenza most likely to be seen in smokers and COPD patients (but not most common). A patient presents with lots of coughing and you’re getting a urine test. To get an abscess. * In long-term alcoholics with lobar pneumonia. levofloxacin. Elderly patient with lobar pneumonia is pneumococcus. then it is strep pneumonia. stroke. If you don’t screen for it with the test. decreased transillumination of sinuses. and exudate. Look at IgG and IgM serology. effusions. confusion. Elderly patient with lobar pneumonia and has COPD or smokes often. the patient must have an increased risk for aspiration and an oral infection. * For anaerobes above the diaphragm we use clindamycin. * Treatment for bronchitis (with sputum) is second or third cephalosporins. levofloxacin. DO NOT DISTRIBUTE . “walking pneumonia. strep. hemophilus. For below the diaphragm we use metronidazole.
what is the next best step? Answer is sputum. not me. the second-line is dapsone. never develop TB. Serology diagnoses Q-fever (coxiella burnetii). No symptoms. has cough. CXR is negative. What about 10mm of erythema? No. -------------------------------------------------------------------------------------------------------------------------------------------Tuberculosis (TB) * 37yo male prisoner at maximum security prison. * What is a positive PPD? 10mm of induration. BCG will not give you 10mm of reactivity. But there is no IV dapsone. PPD is 16mm. but isn’t it better than dying of hypoxemia today? You’d rather be alive with re-activated TB then dead with no TB. What about a 3. short-course steroids for 2-3 weeks will not hurt. * What effect does BCG (Bacillus Calmette-Guérin vaccine) have on these recommendations? None. Now. What about 20mm of erythema? No. “Hmm. iNh. Ethambutol. There are over 2 million in prison in the U. this HIV patient develops the most common side-effect of IV TMP-SMX. the coxiella aerosolizes at the time of birth and they get the pneumonia. * Steroids used if hypoxemia is severe. * Tuberculosis is essentially an economic disease. * Patient has bilateral infiltrates after sniffing a placenta. optic neuritis. where it is 10% per year. Also. That side-effect is a diffuse maculopapular hypersensitivity rash. What is the major side-effects of IV pentamidine? Answer is pancreas problems. It shows an apical cavity and infiltrate. weight loss. PO2 is 65. close contacts. * Say sputum is positive for AFB (acid-fast bacteria) stain. CXR shows bilateral interstitial infiltrates. Sniffing a sheep (Yemenite sheep) placenta. Pentamidine is only second-line if patient has IV therapy. How many drugs should patient’s be started on? 4: isoniazid (INH). Up to 60% of prisoners are PPD positive (tuberculosis). night sweats. found to be PPD positive. Answer is 9 months of INH. pyrazinamide (PZA). negative CXR? What do you do? 9 months of INH. steroid use. and the incidence will rise. * Which TB drug cause hepatotoxicity? Answer is all of them. * Ethambutol affects what organ? Eye. You would need the animal exposure history.” * Any cause of pneumonia can cause hyponatremia. organ transplant recipients. What do you do for this patient? Answer is nothing in asymptomatic hyperuricemia. * What is the fastest way to increase the incidence of sexually transmitted diseases in your community? Answer is bring in a STD specialist into your community. Treatment is doxycycline. PPD is used for screening the asymptomatic. rifampin (RIF). How much risk do you have of developing the disease? Answer is 10% in a lifetime. sputum. what does this mean? It means you have been exposed. Patient has fever. that’s for sick people. Sorry. Except 5mm induration in HIV positive patients because immune system cannot make it to 10mm. For prophylaxis. Without that history. What is the next best step? Answer is treatment. DO NOT DISTRIBUTE . patient is HIV positive with < 200 T-cells.. * 71yo woman who has never been tested. Eye. But isn’t it dangerous to give steroids to someone who is immunocompromised? Maybe. What if the mummy had BCG? 9 months of INH. What? If I’m from India I don’t want to eat isoniazid for 9 months. Severe is PO2 < 70.S. * Neuropathy occurs with isoniazid. Presenting symptom is usually dyspnea. You put the patient in isolation. Anything in the lung can cause SIADH. You check sputum because PPD is not to diagnose acutely ill patients. at any time. Neuropathy. due to ventilation and crowds that you get there. * Abnormal red color with all your body fluids with rifampin. A interferongamma quantification test (QuantiFERON-TB) may be used. So people around animals at the time or birth.Study Notes – Internal Medicine James Lamberg 28Jul2010 * Most specific test for legionella is buffered charcoal yeast extract agar (BCYE). Steroids will increase the inflammation and thus increase the ability to transfer oxygen across the interstitial membrane. ever since this new guy came to town everyone is getting Gonorrhea. Anything in the brain can also cause SIADH. it doesn’t matter no matter how much you think it does. What is the next step in management. you can’t figure it out. cough. for screening populations at risk. asymptomatic.36 - . * On hospital day 2. What is the next best step in the management of this patient? Answer is oxygen. What about 2 meters of erythema? Nope. Rifampin. What is the next best step in the management of this patient.. That means 10 people will get isoniazid for 9 months to prevent that one single case. You give 4 drugs because of the possibility of resistance. Except in HIV. People will be like. That means 90% of people who are PPD positive.791yo Egyptian mummy. Coxiella is the only airborne rickettsia. then give TMP-SMX (co-trimoxazole). ethambutol. * PPD is 5mm induration in HIV. The amount of TB in a country is proportional to the amount spent on public health. How what do you put the patient on? Answer is pentamidine. * Which TB drug causes hyperuricemia? Pyrazinamide. not PPD skin test. Induration is the only important point. they’ll test everyone. Answer is CXR. Red. but it takes a couple of weeks. Antibody testing also takes weeks and is never available to make a treatment decision. * With pneumocystis pneumonia. * If your PPD is positive. INH causes increased urinary loss of vitamin B6.
* Giardia associated with camping and homosexual men. but not when the patient is walking in. This also is associated with wheezing and a rash. septic. If sputum is negative.S. * Which form of food poisoning (diarrhea) causes symptoms the earliest after ingestion? Answer is scombroid. Hepatitis B. yea after you’ve diagnosed it and we culture all the air-conditioning systems. G. This patient got her diarrhea from what she had from dinner the night before or what she had for lunch the day before. If sputum shows TB. * Summary: individual presentation of the patient matters the most. you do a CXR. The only way to distinguish the cause of bloody diarrhea is by culture. It could be campylobacter. Campylobacter is the most common cause of invasive diarrhea in the U. hepatomegaly. B. sardines. HUS. Yea. protozoa. you give INH for 9 months. few cases. like vomiting. sex. staph. B. you give the 4 drugs. you get increased ALT. shigella. Cambodia. malaise. cereus cause symptoms in 2-6 hours. not any form of disease. coli. coli. HepE in the East (SE Asia. weight loss (turns off appetite). watery. * Protozoans. most of the time it does not cause blood. the most important is individual presentation. C. A patient is found to test positive for hepatitis G after a blood donation. Risk factors do not matter if the patient has blood per rectum and a fever. you just caught early reactivation of TB. not shigella. PZA. If CXR is negative. D. Hepatitis G does not cause clinical disease. fatigue. but they found it was C. C. difficile can give you blood. * C. * If you are given no history and bloody diarrhea. because you have to wait for the culture results. Yes. E. it depends on what you eat. Hepatitis G “is a virus with an identity crisis. * If PPD is positive. with a temp of 102 and abdominal pain. WBCs. E. Yersinia. but that is after you’ve already diagnosed it and you did an outbreak investigation. you look for ova and parasites in the stool. not IV drug users. always sensitive). smelly. not E. light stool (bilirubin not in stool anymore). lose weight. but you need to know it. Chinese rice. Laos). * Hepatitis A transferred via food and water (fecal-oral). through food and water. clostridium perfringens is 12 hours. perinatal. salmonella. Your decision point with diarrhea and food-poisoning is blood or no blood. What is the cause of her diarrhea? Not staph aureus. People who living in Wyoming (100% sensitivity to TB medications. HUS is a rare and uncommon association. For salmonella. Shellfish association is Vibrio parahaemolyticus. Test is via toxin. use ciprofloxacin. the last thing you ate is not necessarily the thing that gave you diarrhea. not bacillus cereus. Treatment is metronidazole first. At 6pm. Treatment is anti-histamines. bloody. tuna. make dark urine. Yes. Isn’t erythromycin better for campylobacter? Yes. poopy. association is poultry. mahi-mahi. Legionella and air conditioners. not salmonella. dark urine (bilirubin in urine). Viral is often seen in children. * Also. ethambutol (EMB). not in an individual patient. not vancomycin. E. cereus. Vietnam. and D through blood.37 - . * When you compare risk factors with individual presentation. You treat if they have very severe disease. DO NOT DISTRIBUTE . you check the sputum to make sure you’re not dealing with active TB. * When you have to treat the non-blood diarrhea causes. tiredness. but they predominately present with upper GI symptoms. That is why it is named difficile (Spanish for difficult). Not HIV. The fish eats organisms that make histamine in the flesh. * Who gets the 15mm cutoff for PPD testing? People who should have never been tested in the first place. Can you get hepatitis A sexually? Well. * If the patient is asymptomatic and you get a positive PPD. giardia). or make light stool. RIF. Why not culture? It is difficult to culture. like hypotension. get transaminitis. -------------------------------------------------------------------------------------------------------------------------------------------Hepatitis * Hepatitis A. salmonella/shigella and campylobacter is 24-36 hours. not healthcare workers. what should you tell the patient to expect? Answer is nothing. HIV associated diarrhea is cryptosporidium and there is no therapy and there isn’t going to be a therapy. C. -------------------------------------------------------------------------------------------------------------------------------------------Infectious Diarrhea * 27yo female medical student has a lunch today at 3pm. staph and B. not protozoal (crypto.S. There was a hepatitis F for a little while. HepA is most common in the U. for basic science we learned staph aureus and bacillus cereus is 2-6 hours. INH. but you don’t know if it’s campylobacter. Yes the travelers and undercooked red meat. coli will be associated with thrombocytopenia. not homeless.” It doesn’t make you turn yellow. difficile associated with antibiotics.Study Notes – Internal Medicine James Lamberg 28Jul2010 * Interferon gamma testing is not affected by BCG at all. Hepatitis E (enteric) through food and water. increased bilirubin. It is from spoiled/rotten fish. Most likely cause is campylobacter. diarrhea. then white cells or no white cells. It could not be viral. campylobacter is statistically the most likely. Treatment is metronidazole. she has a big. splenomegaly. but patient has no antibiotics in the history. renal failure. This patient has blood in their stool. febrile. If positive. just normal people. you get INH for 9 months. * What if you do not get blood in the history? Check leukocytes. * With acute hepatitis. not viral.
and treat. hemophilus. even an aminoglycoside. If the vesicles become unroofed. However. * Chronic HepE does not exist. swab. * You do not need to know dose. Same for cervicitis. Treatment could be ciprofloxacin (for gonorrhea) and doxycycline (for chlamydia). ducreyi and with serology for LGV. * Chancroid is painful. * Chronic HepC is treated with interferon and (and) ribavirin.38 - . * Treatment for acute hepatitis is nothing. pancreas) there are 4-5 people waiting. Chronic HepD is treated the same as HepB because you have to have HepB to get D. there is no chronic HepA. combined with ribavirin is 40-50% cure rate. H.S. Treat with doxycycline. What are you going to ask. otitis. Next step is swab. * 27yo man has adenopathy. an HIV retroviral. Interferon alone is 5-15% cure rate. Hepatitis B is the only with surface antibody. this differentiates urethritis. is lung cancer. For every organ that becomes available (heart. you lose some sensitivity because you start to lose antibody over time. If discharge. herpes (HSV). strep. Do serology. * Syphilis chancre is painless and firm/indurated. pleomorphic Gram-negative bacillus. That means you cannot tell just from the serology. so treatment is desensitize and treat with penicillin. DO NOT DISTRIBUTE . gets rid of HepB sAg. Lots of treatments available. In tertiary syphilis. * If you are positive for surface antigen (sAg). bronchitis. so you do the RPR/VDRL then FTA. D. treatment is IM penicillin. ulcers around them. E serology. chancroid is painful and soft. In tertiary syphilis. something like cancer would be carcinoid. What is the next step? Is it RPR. and e antigen. You have to have the time-course with it. IgG chronically. Lamivudine. or any combination. chancroid. try to find intracellular Gonorrhea. treat. Most common cause of cancer death in the world is hepatocellular carcinoma. * Vaccination against HepB gives you surface antibody only. lung.S. Most common in U. * In real inflammation. C. have you had sex with any yellow people recently? There are 5 types of hepatitis with 2 transmission methods and 1 presentation. VDRL? Only about 75% sensitivity with VDRL and RPR in primary syphilis because it needs time to make an antibody response. * Neurosyphilis takes about 10 years to develop. something like leukemia would be leukemoid. What is the next best step in the management of this patient? Answer is treat herpes simplex with acyclovir. treatment is IV penicillin. Tertiary syphilis. * Treatment is ceftriaxone (for gonorrhea) and azithromycin (for chlamydia). urethritis. you are infectious. painless and firm ulcer. chlamydia. * It helps memory to think about what this actually means. * Azithromycin is fantastic. but you do need to know route of administration. just so you cover both gonorrhea and chlamydia. IgM acutely. like meningitis. Ribavirin/interferon can help prevent the most common cause of liver transplantation in the United States.Study Notes – Internal Medicine James Lamberg 28Jul2010 * Patient presents and is yellow. so serology with just positive sAb is vaccinated. anything will pass through the BBB. HepC is the most common reason for needing a liver transplant in the U. famciclovir. MAC. covers chancroid. initial test is a dark field. core antibody. How do we tell if it is urethritis or cystitis. looking for cellular atypia. Decision point is painful versus non-painful. doxycycline will not cross the BBB very well. or valacyclovir. meaning they get rubbed and the top comes off showing an ulcer. * 27yo man comes to clinic with multiple small painful genital fluid-filled vesicles. Answer for treatment is single dose azithromycin. cervicitis. ducreyi. because it has greater sensitivity for primary syphilis. sinusitis. culture. Stain. “-oid” means similar. surface antigen. Ask if there is discharge. * 27yo man comes to clinic with genital ulcer and adenopathy. * Core antigen could be positive or negative. * Chronic HepB is treated with interferon or (or) lamivudine. then you do a Tzanck and culture with Gram-stain for H. but about 1 year in HIV patients. * Primary and secondary syphilis. staph. Lamivudine is an oral pill to prevent the most common cause of cancer death in the world. VDRL and RPR are at 100% sensitivity. and lymphogranuloma venereum (LGV). * Mycobacterium avium prophylaxis with a single weekly dose of azithromycin. * What is patient is allergic to penicillin? Answer for primary/secondary syphilis is doxycycline. -------------------------------------------------------------------------------------------------------------------------------------------Sexually Transmitted Diseases * Patient presents saying their penis is burning. core antigen. how long was your asymptomatic incubation period. Once you get to secondary syphilis. Tzanck smear involves swab and putting on slide. liver. * Desensitize and treat with penicillin in pregnancy as well. You see the genital vesicles. try to look for Gram-negative diplococci. How do you distinguish via history and physical exam which type of hepatitis we have? You can’t. has urinary frequency. Presentation seen in syphilis chancre. * Syphilis is rarely seen in our population. The FTA-ABS does not go away. it doesn’t determine if HepB is chronic. Chronic HepA is treated with nothing. You won’t find a dark field scope anywhere. * Acute or chronic is determined by the surface antigen being present beyond six months. so you do not need to Tzanck prep. * LGV is big beefed-up matted up lymph nodes. * Diagnosis is via anti-hepatitis A. culture. Testing can be done with Gram stain and culture.
strep and sometime staph. pregnant. * Cystitis treated with TMP-SMX or ciprofloxacin for 3 days. cloxacillin. dig.39 - . azlocillin. Usually length of treatment is a matter of local tribal customs. Answer is impetigo. tumors. fluoroquinolones. That is interferon in your body. That could be aminoglycosides. stain. You get the same symptoms with the flu. -------------------------------------------------------------------------------------------------------------------------------------------Skin Infections * Scabies. strep pyogenes. you can’t Gram stain an ultrasound. Answer is erysipelas. No matter what the standard of care is. dysuria. Bacteria in the urine is only significant in one patient population. Is there an anatomic defect (stone. irritability. If you have a mild penicillin allergy then use first-generation cephalosporin. What is the most common side-effect of digoxin. Molluscum contagiosum gives warts with an umbilicated center. melt. The problem is this happened while you were on antibiotics. So if you’re writing board questions and you choose side effects to ask about. diuretics. The most accurate test for abscess biopsy or aspirate. treatment is to drain the abscess. caused by strep. cut. what do you use? Answer is oxacillin. hydronephrosis)? * Say you put patient on antibiotics and 3 days later they are still sick. freeze (cryo). depression. oozing. dicloxacillin. Most important thing to look for is WBCs. You can’t get rheumatic fever from this. or other anatomic complication. -------------------------------------------------------------------------------------------------------------------------------------------Cystitis & Pyelonephritis * 39yo women with urinary burning. Poxvirus gives small little warts. Staph epidermidis lives on your skin and therefore does not cause infections of the skin. Test is visual identification of wart. you can’t get sensitivity on an MRI. ampicillin. Now we know dig is lousy and does not decrease mortality. chop. aztreonam. because you make interferon yourself. Treatment is lindane or permethrin. urgency. * What is the most superficial of all the bacterial skin infections involving just the epidermis? Weeping. Might see trails dug under skin in skin creases. So now treatment is ACE-I. In 1985 for a short time we used hydralazine and nitrates. So. 5 times smaller than lice. Is this cystitis or pyelonephritis? It is the same for both. just remove it. If lifethreatening penicillin allergy. Staph here is staph aureus (not staph epidermidis). frequency. * Which skin infection involves the epidermis and extends into the dermis? Causes swelling in dermal lymphatic channels and bright-red skin. You use the ultrasound because you know the patient has pyelonephritis and want to see what the cause is. crabs if genital) is found near hair areas. 7 days is for stones. tumor. 3 days for uncomplicated. Lice (pediculosis. GI symptoms (nausea. * Which skin infection involves the dermis and subcutaneous tissues? Answer is cellulitis. pregnant patients. The strep in these skin infections is group A beta-hemolytic strep. Best initial diagnostic test for both is urinalysis. sarcoptes scabeii. He’s digging and pooping. whatever. nafcillin. dig. Treatment is remove. 1/3 of women with bacteria will develop pyelonephritis. preterm delivery associated with bacterial vaginosis. you won’t have to edit questions much in the future. Treatment is lindane or permethrin cream. None will cure the virus anyway. like cryo would).g. Diagnostic test for warts not smear. You can’t stain a CT. Cough with ACE-I. diuretics. contact dermatitis. There is no specific drug. beta blockers. staph and strep. Cystitis is such a routine problem that there is a standard length of therapy. vancomycin or macrolides. Fever can help a little too because there is a little fever in cystitis and big fever in pyelonephritis. * An ultrasound looking for pyelonephritis will show nothing. pains. * Pyelonephritis is a drug that covers Gram-negatives. burn. So care was ACE-I. just pick what covers Gram-negatives. vomiting). honey-colored crusting of skin because it lifts up the epidermis. It stimulates the T-cells to react to the wart as foreign and sloughs it off. -------------------------------------------------------------------------------------------------------------------------------------------Medication Side-Effects * Interferon major adverse effect is flu-like symptoms. It does not get to the dermal-epidermal junction so it cannot cause oozing above skin. strictures. biopsy.Study Notes – Internal Medicine James Lamberg 28Jul2010 * Patient has genital warts (condyloma acuminata). diuretics. Now what is the next step? Ultrasound or CT or MRI and you find an abscess around the kidney. We found hydralazine wasn’t as good as ACE inhibitors. DO NOT DISTRIBUTE . * Do you have to drain the abscess or can you treat with antibiotics? Most of the time you drain abscesses. the adverse effects will not change. treatment of CHF would be digoxin and diuretic. ticarcillin. There is itching because of the eggs and feces. but you can get glomerulonephritis. Suprapubic pain in cystitis and flank pain in pyelonephritis. Diagnostic test is scraping. * Interferon causes aches. You can tell these apart by the pain. Why do board exams emphasize adverse effects? Say we’re in 1970. swab. Imiquimod is a local immunostimulant and the only treatment that does not go too far and burn the skin (e. * Best diagnostic test for cystitis and pyelonephritis is a culture. * If you’re not sure what type of skin infection this is. piperacillin.
* Mold treatment with hair/nail involvement cannot be topicals. If MRI or bone scan is positive. The most accurate test for any infection is culture (few exceptions. KOH melts away the epithelial cells. good for cryptococcus. If the x-ray shows osteomyelitis. tender. miconazole. It is the only one you can treat with topicals because it is superficial. swollen. oral thrush. So you do not know what organism to treat. only worked 30-40% of the time. yeast in the beast. can also give itraconazole. then this is just an ulcer. red. Treatment is based on whether or not there is hair/nail involvement or no hair/nail involvement. You don’t skip an ECG and jump straight to the stress test. Oral thrush. econazole. dermatophyton. not osteomyelitis. then what is the next step? Answer is MRI. it is the same stuff that makes the lobster/crab shell hard. It will not tell you what is in the bone. inside the group are molds and yeasts. hot. lotrimin.” Only mold to worry about in general is skin infections. Inside you at body temperature is yeast. You start the patient on 6-weeks of antibiotics after the biopsy. but do the x-ray anyway. It will be contaminated and colonized with skin flora. * When do you culture the drainage out of the sinus tract? Answer is never. Doesn’t it take 2-3 weeks for the bone to dematerialize enough to see it on an x-ray? Yes. If the SED rate is down then you can stop. effusive knee. which is why you do the biopsy. * Molds include epidermophyton. * If x-ray and MRI negative. Kid comes with toenail infection. vaginal candidiasis. * What if the original x-ray were negative. * The KOH will show the fungi. periosteal elevation. You follow the ESR. Others would be risopus and mucor mycosis in diabetics. How do you know what organism to treat? Most common cause of osteomyelitis is staph aureus. It hurts just below his knee. clotrimazole. terconazole. * Do not culture sinus draining tracts due to false positives. most common side-effect is gynecomastia. Rubor. ketoconazole. microsporon. * X-ray shows osteomyelitis. then look at the slide. next step is biopsy to determine organism. It does not work on molds. diabetics are more susceptible to Gram-negatives and anaerobes. culture? Answer is x-ray. miconazole. * Fluconazole is a yeast drug. heat it up.Study Notes – Internal Medicine James Lamberg 28Jul2010 * Impetigo can sometimes be treated with topicals like bacitracin or mupirocin. What is the best initial diagnostic test? CT. X-ray very rarely shows anything in septic arthritis. Ketoconazole also affects the liver due to P450 interaction. Molds (e. like herpes encephalitis with PCR). then treatment. malassezia furfur. destroyed bone involucrum and sequestrum. However. this way you do not need to do a bone biopsy every few months. Fungi has chitin in the cell wall of the fungus.40 - . Articulatory cartilage is amazing stuff. * Griseofulvin had to be used for 12-18 months for nail infections. * Mold treatment without hair/nail involvement would be any topical. Environment growing in the refrigerator or plants tends to be molds. She has a painful. then after 6-7 weeks or so you check a SED rate. Fluconazole is very safe. like athlete’s food. * When do you get a SED rate? You get it to follow the response to therapy. athlete’s foot spreading. Must be systemic therapy. Answer is aspiration. Do not do a bone scan because the red ulceration soft tissue swelling gives too many false positives. X-ray is always first with osteomyelitis even if you think it will be negative. X-rays. MRI has same sensitivity as bone scan but does not come with the false positives. it is very close to orchiectomy at high doses. bone scan. even in rheumatoid arthritis. put some KOH on it. cryptococcus are yeasts. fingers for 6weeks. Scrape area. nystatin. tumor. SED rate is useful to determine length of therapy. -------------------------------------------------------------------------------------------------------------------------------------------Osteomyelitis * 57yo male diabetic with peripheral vascular disease and has pain in leg for last 10 days. -------------------------------------------------------------------------------------------------------------------------------------------Septic Arthritis * 72yo female Catholic nun from Brazil with a fever. What is the best initial diagnostic test.g. The only way to know which specific fungus is to do a culture. “Mold in the cold. even if the person has only had the disease for 5 days. MRI. 80-90% cure. * Fungus is the group. use ESR. calor. * We don’t use ketoconazole usually. leaving fungi. have a 6-month lag time. dolor. It is very anti-androgenic that systemically you are more likely to use it for metastatic prostate cancer. Never wait for results of culture to treat. x-ray. immobile. What is the next step? Answer is biopsy. -------------------------------------------------------------------------------------------------------------------------------------------Superficial Fungal Infections * Any form of superficial fungal infections has the best initial test of KOH and culture. So get the culture then initiate treatment. vaginal candidiasis. if the SED rate is still up then you continue. Treatment for 12-weeks. takes DO NOT DISTRIBUTE . athlete’s foot) take weeks for the cultures. Some people may need 4-6 months of therapy. some acetic acid. yeast/candida in blood. Cellulitis with red draining tissue will mess up the bone scan. has an ulcer over the area over past 5 days with a draining sinus tract. terbinafine.
hemicolectomy. Osler invented residencies in this country and wrote the first comprehensive medical text. pharynx positive in 10-20%. then you know this is endocarditis. No dose after the procedure.Study Notes – Internal Medicine James Lamberg 28Jul2010 huge amount of stress and trauma. the papillary muscle and chordae tendineae will not jump out and reattach themselves. do a Gram stain. 700 pages. culture everything. Less than 10% of patients have any of these signs. it DO NOT DISTRIBUTE . Gram-positives with something like oxacillin. do not order scans here. get the blood culture. These patients dies of post-infectious endocarditis. get echo and you’re done. dental cleaning) and a significant defect (e. whatever. TTE will miss almost half of endocarditis. Now what? MVP. * Sensitivity of TTE is 50-60% sensitive.000 white cells. aortic stenosis. rheumatoid factor negative. CABG. When do you wait for results of culture? Never. There is not specific drug to learn (like ceftriaxone in meningitis). You won’t get asked diagnosis. That is why you order blood cultures first. increased motilin). I just lay there. How do we make the diagnosis then? Rectum positive in 1020% of patents. give clindamycin. mitral stenosis. culture positive in only about 50%. Are you sexually active? No. You look in this guy’s eyes and see no Roth spots. arthrocentesis.g. No Janeway lesions. So you have some heart problem and are getting a bacterial flinging surgery. does not cause bacteremia. no prophylaxis needed. cervix positive in 20-30% of patients. So for non-gonococcal septic arthritis. * Say arthrocentesis shows 62. Urine has no red cells. If blood cultures are positive. Treatment is ceftriaxone. Culture of synovial fluid is over 90% sensitive. so not used primarily. IV drug use. but that is pretty invasive. or pacer in place. has fever. TEE is more than 90% sensitive. If patient is penicillin allergic. What is going to tell you to do all these cultures? Is there a rash (non-blanching petechial rash) that goes along with neisseria infections? Migratory polyarteritis. * Many physicians will not even take a sexual history because they assume it is unreliable. * You’re going to get your teeth cleaned and have MVP. All you need to see is fever and a new murmur. Synovial lining does not have a basement membrane. bacteria cannot penetrate. give prophylaxis if significant regurgitation (murmur). Erythromycin will cover the mouth flora.g. Osler lived 50 years before antibiotics were invented. biliary surgery. but has side-effects (vomiting. uterus is sterile environment. Gram-negatives with something like third-generation cephalosporin (ceftriaxone). so bacteria (and antibiotics) pass easily. What type of septic arthritis does this patient have? You have to order tests. nafcillin. * Prophylaxis for general procedures like dental work is amoxicillin 2grams one hour prior. -------------------------------------------------------------------------------------------------------------------------------------------Endocarditis * 27yo man. So again. aortic stenosis. * What about gonococcal septic arthritis? Blood positive in less than 10%. Now the most common cause of death from endocarditis is CHF. Pacemaker. polys. no prophylaxis. azithromycin is alright. mitral stenosis. polyarthralgia (in multiple locations)? Tenosynovitis? That is how you know. 20% gram negative rods. What is the most accurate diagnostic test for this patient? Answer is culture. You look in this guy’s fingers and see no splinter hemorrhages. needs prophylaxis because it is significant enough to cause sudden death. If negative. IVU (IV drug use). all these areas. and murmur. * Summary: you see fever and murmur. even after blood cultures. hemicolectomy. then get transesophageal echo (TEE). and considering it is 97% water. and joint pain. quinolones. we’re going to find it. VSD). What does that mean? Nothing. you need a bacteremia causing procedure (e. fever. -------------------------------------------------------------------------------------------------------------------------------------------Lyme Disease * A bunch of children are brought to the hospital with rash. even though it is a foreign body. Take culture and start to treat. ANA negative. What is the sensitivity of a Gram stain? At least 50-70%. * Treatment is with two agents to cover Gram-positive and Gram-negatives. * What is the next best step in the management of this patient? Blood cultures or echocardiogram? Answer is blood cultures. cystoscopy. You look in hands and feet and see no Osler nodes. CABG. if you think there is gonorrhea. If TTE is positive. IHSS (HOCM) idiopathic hypertrophic subaortic stenosis. then get transthoracic echo. Gram positive in less than 25%. If TTE is negative. urethra positive in 10-20% of patients. * To get endocarditis. only 40% of disease had treatments. do an aspiration. just cover bacteria present. Prophylaxis for endocarditis when something is on the inside. When do you answer surgery? What is the most important and urgent indication for surgery in endocarditis? Answer is CHF. SED rate a little elevated (and SED rate is like Rorschach inkblot test. this is how we think about metastatic disease. Cardiac catheterization (with valve problem). * Treatment is started right away. no prophylaxis needed. In 19th century. The physicians do tests. C-section (with valve problem). coronary arteries are on the outside of the heart. tap the knee. Blood cultures positive in 25-30%. 10% misc. No matter how long you give antibiotics. So. * Dr. * Non-gonococcal septic arthritis. most often staph (40%) and could be strep (30%).41 - . no prophylaxis. Only single disease with 100% mortality was endocarditis.
meaning T-cells from > 500 down to < 200? Answer is viral load. zalcitabine (DDC). Viral load tells the future. CMV with oral ganciclovir also not used. -------------------------------------------------------------------------------------------------------------------------------------------Human Immunodeficiency Virus (HIV) * Asymptomatic patient with HIV presents to your office asking what medications they should be taking. * Diagnosis is clinical manifestation. 15000 cases per year and it is very hard to die from. prophylaxis with TMP-SMX. Second highest incidence of Lyme in Westchester NY which has the 2nd highest per capita income in the world. what should he be started on? Answer is TMP-SMX and azithromycin? * What vaccinations should an HIV positive person be on? Answer is influenza annually and pneumococcal. No need for tick analysis. What determines what length of time you develop AIDS. * Less than 200 T-cells and less than 50 T-cells is what you need to know.Study Notes – Internal Medicine James Lamberg 28Jul2010 doesn’t mean anything). Bell’s palsy). use ceftriaxone. You don’t feel 400 or even 350. Lyme in Connecticut (near Yale. there is a Lyme vaccine. based on T-cell count of viral load? CD4 under 350 or viral load over 55000. Moms look into their pediatrics textbook of medicine and decide to stop back to the doctor’s office the next day. at risk for mycobacterium avium intracellular (MAI. you do not have Lyme. Prophylaxis is based on what you are at risk of today. * The fascination from Lyme comes from parents coming back and back and back until the disease was described. They kill a virus so we call them -avir. Then what? Do nothing. It has a high incidence with the wealthy population. HIV drugs. If cardiac or neurologic problems. and some neurologic problems (e. nelfinavir. Didanosine (DDI). Physicians send kids home and say children have juvenile rheumatoid arthritis. * Protease inhibitors were created de-novo. patients were taking pills all the time but still dying anyway. * Zidovudine (AZT) causes anemia. 95-98% of patients who are HIV positive without treatment will die from AIDS. But. No need to treat. Worry when you get near 200. What do you do for this patient? Answer is tickectomy. Serology for IgM and IgG is lousy because it cannot distinguish well between old and current infection. how aggressive the diseases is. but can get nasty arthralgia later on. She has no symptoms. Characteristic about CN VII palsy is that it is bilateral Bell palsy. or just the neuro. You do not treat asymptomatic serology. Is prophylaxis based on the T-cell count or the viral load? Answer is T-cell count only. With these 5 medications. Rifabutin is a dead drug. The rate of decay of T-cells is dependent on the viral load. Lamivudine (3TC) has such few side-effects that the placebo has more side-effects during testing. for minor stuff like rash or Bell palsy or joint problem. * 50 T-cell or less. or just any of them. protease inhibitors. This is how Lyme disease was described. serology is useless for Lyme. Mortality on Lyme is negligible.g. Patient may get a rash sometimes. MAC). * Use 2 nucleosides and a protease inhibitor (PI) and viral load goes to undetectable in 80-90% of patients. All the children in an area won’t get JRA at the same time. * When to start HIV medications. not by screening thousands of compounds. cardiac problems. It’s like a train heading toward a cliff. 3rd highest income per capita in world). * 200 T-cell or less. reverse transcriptase inhibitors. use dapsone. Without clinical manifestations. and that is the problem with diagnosis today. Side-effects of DDI and D4T are neuropathy and pancreatitis. Reverse transcriptase inhibitors are -vudine drugs. saquinavir. Lyme. Indinavir. The T-cells tell you how far the train is away from the cliff and the viral load tells you how fast the train is moving toward the cliff.000 cases per year and practically no one dies. and when to start anti-retrovirals. If you get a rash. This means you cannot die from the virus. * Treatment is doxycycline or amoxicillin. Normal is around 600-1000 T-cells. remove the tick. No need for serology (positive serology wouldn’t matter). 3-30 million people go blind annually because they don’t have a dollars worth of doxycycline or erythromycin. how fast will T-cells drop. Third line is atovaquone. * Tick ixodes scapularis has to be attached for 24-72 hours. this is not like syphilis with VDRL and RPR (diagnosed with syphilis even if no symptoms).42 - . stavudine (D4T). You can get just the rash. T-cells tell the present. at risk for pneumocystis pneumonia (PCP). Positive blood test with no symptoms means no Lyme. ritonavir. * There is no malaria vaccine. DO NOT DISTRIBUTE . * 26yo woman who gets bitten by a tick on her buttocks. You can get joint problems. * No mortality benefit with antifungal prophylaxis with fluconazole. Aerosol pentamidine is 4th line and practically an extinct drug. If you have a positive serologic test and no symptoms. 15. * Asymptomatic HIV-positive man comes to your office with 12 lonely T-cells. These are very effective. possibly a few AV block cases. * About 5% of patients who are HIV positive will never develop AIDS. There is no chlamydia trachomatis vaccine. prophylaxis with azithromycin.
What do you do for this patient? Answer is 2+1 now. event. so quickly review an image for each disease discussed. stop medications. Answer is not surface area differences. there are about 5 drugs created for tuberculosis. load. -------------------------------------------------------------------------------------------------------------------------------------------Bullous (Blistering) Diseases * Pemphigus vegetans is a rare variant of pemphigus vulgaris. Risk of transmission through breast milk is equal to unprotected sex or equal to the risk from the delivery itself. how long do you continue the medications? If you keep patient on medications for 5 years. * Risk of transmission is about 1:3000 for female to male (vaginal). what. * When the antibodies attach to the antigens. * 33yo man has unprotected sex with an HIV positive girl. You took a fatal prognosis with HIV. * Pemphigus vulgaris is a blistering disease. they’re on it for 3-months. DO NOT DISTRIBUTE . and it breaks apart and blisters up.43 - . This woman has a 50% six month mortality. So. * Put patient on 2+1 therapy. -------------------------------------------------------------------------------------------------------------------------------------------HIV Transmission Risk * 32yo woman who is pregnant and is HIV positive.. and made it 80-90% not fatal.000.R. Have gratitude in your attitude for access to the medical therapy we have. transmission rate drops even further to about 2%. but most of the skin will be denuded. comes back with terrible flank pain and hematuria. Man is only exposed for about. -------------------------------------------------------------------------------------------------------------------------------------------Kaplan Videos (2001) – Dermatology with Dr. * Why is male to female transmission higher than female to male? Answer is not vaginal trauma. they are undetectable. they are very fragile and easily breakable. average life expectancy for a woman is 79 years. death rate is higher since there is no milk formula available. What is the next best step in management. -------------------------------------------------------------------------------------------------------------------------------------------Post-Exposure Prophylaxis * 26yo surgical intern is stuck with an HIV positive needle (needlestick) in the O. So how much has the death rate from HIV dropped in the United States? Answer is 80-90%. Average life expectance of an HIV positive person who gets the disease around the age of 40 is the same as an HIV negative person provided they get the 2+1 therapy. 10 seconds? The time duration of the coitus. * 27yo woman is sexually assaulted by an unknown man with unknown HIV status? What medications do you give her? Answer is 2+1 for one month. Needlestick exposure is about 1:300 episodes/contact. What is the next best step in the morning? Answer is give 2+1 for one month. Risk is about 1:1000 for male to female (vaginal). In Africa. * Once you start HIV medications and you go undetectable. Answer is give 2 nucleosides and 1 protease inhibitor for one month. C-section not routinely indicated. viral load of 600. causes stones. Patients with pemphigus vulgaris have auto-antibodies that respond to antigens that are found in the epidermis (top layer) of the skin. the skin can no longer stay intact. by her attending physician. who tells him afterwards. The blisters are so superficial that by the time the patient presents to the physician you rarely see intact blisters. She is at 7 weeks of pregnancy. If you do see intact blisters. Her T-cell count is 35. Oral transmission rates are not really known. it is a difficult thing to study. You start HIV medication for < 350 T-cell or viral load > 55. 16 HIV medications were approved and new ones coming out all the time. Mother to child transmission is about 1:20 with meds and about 1:3 or 1:4 without medications. Answer is duration of contact with infected semen for 4-5 hours. Marsha Gordon.S. less than 4-5 hours. Anal receptive is about 1:100 (1%) per shot. Half of those children will be infected and most of those children will be dead by age 5. * In the United States. You’d rather be alive with a high LDL and HbA1c then dead with normal levels. Over 10 years. Do not let her die because she is pregnant.000. Which drug caused this? Answer is indinavir. it is 32 years. * Protease inhibitors have side-effects of hyperglycemia and hyperlipidemia. mainly due to the fact that 1/3 of women in prenatal clinics are infected with HIV.Study Notes – Internal Medicine James Lamberg 28Jul2010 * So protease inhibitors help drop viral load to undetectable in 80-90%. MD -------------------------------------------------------------------------------------------------------------------------------------------This section is very picture-intensive. These antibodies are found in the intercellular spaces between epidermal cells. * Over 70 years. In South Africa. Pemphigus vulgaris is an autoimmune disease of the skin. only if viral load is not under control. * Pediatric HIV is virtually non-existent in the U. less than 400 children born HIV positive. and that is a great good. With 2+1 therapy. the virus can come back the next day. You took a transmission risk of 50% and brought it down to 2-3%. * AZT alone in pregnancy results in about an 8% transmission of HIV. patient is on medications forever. * Which HIV medications (nucleosides or PI) are teratogenic? None of them.
causing hive swelling. This is believed to be a type IV hypersensitivity eruption. * If a patient is given an antibiotic and are doomed to develop a morbilliform rash. and fungicide hexachlorobenzene may be a precipitant. It almost exclusively involves the mouth and eyes. think pemphigus but realize the actual diagnosis is made by biopsy. They almost never present with intact blisters. If you see a slide with blisters and denuded areas. As a result. the blisters are deeper. lymphocyte mediated. It is believed that this is the time needed to recruit and sensitize the lymphocytes. It is mast-cell induced. This is important because other diseases can look like hives. Skin that is exposed to the sun. Erosions in the oral mucosa may occur before skin is involved. * Morbilliform eruption is a faint pink morbilliform (measles-like) eruption. they look like they are getting a tan. scars around mouth. so middle-aged alcoholic with blisters. you will get an urticarial reaction probably within 30 minutes to an hour at the most. * There will be intact. If the urticarial hive lasts less than 24 hours then it is urticaria. * Two other skin manifestations besides blisters. the first time they are exposed they will not develop a rash from somewhere between 10days to 2weeks. at the DE junction. * Clinically we see blisters and erosions. classically the dorsum of the hands. -------------------------------------------------------------------------------------------------------------------------------------------Porphyria Cutanea Tarda * All porphyrias relate to abnormalities of heme metabolism. * Cicatricial pemphigoid is a less important variant and does scar even with treatment. * Porphyria cutanea tarda (PCT) is the classic dermatological porphyria. they become hairier. so women who are on birth control pills or hormone replacement. develops a photosensitivity. a linear line. * Bullous pemphigoid biopsy will show blister with entire epidermis lifting and separating from the dermis. We also treat with blood-letting (phlebotomy) to try to drain off excess iron. * These are immediate reactions. it attaches to IgE antibody on the mast cell and causes release of the mast cell package. tend to be tense. The metabolites that accumulate are photosensitizing. Iron may be a precipitant. * Bullous pemphigoid presents in an older population. * Any individual hive will last up to 24 hours. It is a slow improvement and may take up to a year. * Morbilliform drug rash often seen with antibiotics. They do not react with anything in the epidermis per say. The blisters are tougher. DO NOT DISTRIBUTE . it heals with scaring and heals slowly.Study Notes – Internal Medicine James Lamberg 28Jul2010 * This disease affects the skin and the oral mucosa. This condition does not heal well. * Bullous pemphigoid is an autoimmune disease of the skin with antibodies reacting against antigens at the dermoepidermal junction zone (DEJZ). You see leakiness of the vessels. This does not generally involve the oral mucosa. and also immunofluorescence can show the antibodies being deposited in little circles around the epidermal cells. they react at the DEJZ. * Precipitating factors for PCT is alcohol. they develop hypertrichosis. tense. * The second exposure will result in a reaction within 3-4 days because they have been sensitized. Bullous pemphigoid is seen in a geriatric population classically. -------------------------------------------------------------------------------------------------------------------------------------------Hypersensitivity Reactions * Urticaria is the classic type I hypersensitivity eruption. steroids. The classic place the hair is seen is at the tops of the cheeks. blisters with some denuded/eroded areas. now we treat with high dose prednisone and steroidsparing medications like azathioprine. * Biopsy must show the epidermis breaking apart one cell from the other. However. meaning if the patient is allergic to penicillin and you give them penicillin. a differentiating feature between the two. blindness from eye involvement. Immunofluorescent will show lighting-up. The disease was fatal prior to discovering corticosteroids. Mast-cells have IgE antibodies affixed to them. causing hive pinkness.44 - . The top of the scalp is another location. including lots of histamine and mediators. ages around 70-80. * You see vasodilatation. * Pemphigus and pemphigoid tend to heal well with treatment. * The face also can be involved. Pemphigus presents classically around ages 30-40. and when proper allergen comes along. It may be slightly raised. Second. First. so scarred tongue. * Pemphigus foliaceus and pemphigus erythematosus are more superficial forms of pemphigus. new hives will continue to present over weeks as long as the antigens are present in the system. and often are intact when they present. patients develop hyperpigmentation. * Many disease present looking similar to pemphigus vulgaris. * Treatment is to remove precipitating factor and use anti-malarial medication chloroquine. Estrogens are a classic precipitant.
but don’t forget it could be a tinea corporis. Within a short period of time. The infection can get down into the roots so topicals will not reach. usually involving the soles of the foot. Whatever the formation. think impetigo. barbiturates. the break is way high up in the epidermis. May have fever. you will see the honey-colored crust and blisters around. * The multiforme means it can take many forms. The blisters have purulent material in them and are teeming with staph. red.g. * On frozen section. If you give the drug back. The entire thickness of the epidermis is lifted and separated from the dermis and is necrotic/dead. Say patient has impetigo that is caused by one of these types of staph (bullous impetigo). scaly border. older or very young. Mortality 25-50% even with appropriate treatment. This toxin can cause the skin to blister. Caused by staph or group A strep (pyogenes). * Fungal infection of the toenails is onychomycosis. in the exact same location. but the main site is distant from the skin (e. the same reaction occurs. targetoid appearance. and finally to toxic epidermal necrolysis (TEN). * Erythema multiforme is self-limiting. * If any mucus membrane involvement. patient is prone to infection. Tinea cruris is fungal infection of the groin. watch fluid and electrolytes. If you can’t tell the difference. abdominal abscess). Sometimes the skin is scaly and peeling. * Tinea corporis can be very subtle with a tiny pink scaly area. must have an ophthalmologist involved in this care. allopurinol.Study Notes – Internal Medicine James Lamberg 28Jul2010 * Spectrum of hypersensitivity reactions begin with erythema multiforme. we see complete necrosis of the entire epidermis. a recurrent infection. * Fixed drug eruption generally heals with a dark mark that can take a long time to fade. * Erythema multiforme often seen to drugs and also infection (herpes and mycoplasma pneumonia). * Treatments involve covering for staph and for strep. In SSS. do a culture (takes weeks) or a KOH prep. * TEN can look very much like staphylococcal scalded skin (SSS) syndrome. * There can be 100% sloughing of skin. * Treatment of tinea capitus is oral anti-fungals. * Disease can last 2-3 weeks. * Stevens-Johnson refers to more than minor mucus membrane involvement. If you take away the drug. we do a biopsy and send it for frozen section because we want an answer quickly. Tinea pedis classically involves the interdigital webs between the toes. With skin involved. Classic example is a bull-shot with a dusky bluish color in the center and a red rim around. then to Stevens-Johnson. * TEN prone to electrolyte abnormalities and infection. Think about this if called to a neuro management unit for a major skin disorder. We do not know why this happens. DO NOT DISTRIBUTE . they can be seen on other parts of the body. they develop either a blister or a red mark. Because the patient is debilitated. carbamazepine. giving a permanent scaring alopecia. poor kidneys or poor liver. Many times you will think this is just an eczema. This is almost always caused by a drug. In one are. * To make a TEN diagnosis. the skin begins to bubble-up and literally sloughs off. Tinea capitus can scar if not treated. so like a 100% burn. put in laminar flow room to prevent infection. elevated liver function tests. These patients are tremendously ill. pus bumps. The blisters are intact and if you open and do a KOH prep you will see it teeming with dermatophytes. phenytoin. Because eye involvement can occur. Specifically with herpes. but is treated very differently. There is a blistering form of tinea pedis. thus will go away if you remove the offending agent/disease. With mucosal involvement. * Honey colored crust. * Toxic epidermal necrolysis involves skin that is confluently red that burns or feel tender. * TEN treatment is stop medications. patient can get recurrent erythema multiforme with each outbreak. -------------------------------------------------------------------------------------------------------------------------------------------Bacterial Skin Infections * Tinea pedis (fungal infection of foot) caused by dermatophytes (fungus that attacks the skin). These patients will likely have skin involvement as well. Classically involves the palms and soles. it will be target-like. Say in addition the patient is pretty sick. However. the involvement has to be very minor to be called erythema multiforme. * Tinea capitus usually seen in kids with a patch of hair loss (alopecia) or thinning. So you see fluid and electrolyte abnormalities. it is just a curiosity. sulfonamides. elevated white count. extending over time. while TEN can be caused by antibiotics. Classically you see hemorrhagic crusts of the lips and oral mucosa. So there may be a blister in the center with a red rim around. steroids are highly controversial because they mask infection. patient may not be eating well. Classic pattern is annular (round). exfoliatin. Sometimes there will be a few little pustules. * Stevens-Johnson has a mortality of 5-10% even with appropriate treatment. they cannot break down this toxin and it spread throughout the body. classically seen on the palms. bullous tinea pedis.45 - . Treatment of SSS with antibiotics. cortisone (prednisone). * Erythema multiforme refers to target-like lesions. * Certain strains of staph exude a toxin. which is a major cause of death in TEN. * Staphylococcal scalded skin syndrome is from staph that exudes exfoliatin toxin. it heals. * Fixed drug eruption refers to a situation when a patient is exposed to a drug they are allergic to. penicillins. It is benign.
often arising in times of stress. tinnitus. hard. * Herpes comes and goes. Usually pretty evident. The average time when the blood test turns positive is 4-weeks. Presents with red. This is shingles from herpes zoster. Some believe you need an LP. * Here you do a frozen section to differentiate from TEN. A day later. Average time of onset of chancre is 3-weeks after exposure. Lips can be very swollen. * Meningococcemia present with a brief upper respiratory infection. There is no way the antibiotic will get into the necrotic tissue at the fascia in time unless the area is completely and widely debrided. associated with nontender adenopathy. a reactivation of latent varicella zoster virus (chickenpox). nontender classically. Itchiness due to stool. the blisters begin to develop. think about Ramsey Hunt. you see intact epidermis expect for very superficial blistering. * Furrows or linear burrows may be a clue. we can do a biopsy and see strep very deep. Next stage is a fever and mental status changes. can be from 10-90 days. Other places classically involved are breast. So if you see the patient and think it is a chancre. At this point. If can be so acute and fulminant that there isn’t enough time. If TEN. * Necrotizing fasciitis (flesh eating disease) is a medical emergency. Not much to say about warts. -------------------------------------------------------------------------------------------------------------------------------------------Other Skin Infections * Scabies is caused by human mite. * Patients need a good general workup for any herpes zoster a month after healing because they may be immunosuppressed for a variety of reasons. extending down a dermatome. where they can spread across the planes and cause damage very quickly. warm. * Treat necrotizing fasciitis with antibiotics and it absolutely requires surgical debridement. Superficial at the granular layer of the skin. * Secondary syphilis appears 6-8 weeks after chancre. CN VIII. * Think about any other bacteremia here also. * If trigeminal ophthalmic division is involved with herpes you need an ophthalmologist. This patient is not controlling their zoster infection Admit patient to hospital and treat aggressively. * Herpes zoster is disseminated if more than 20 blisters outside of a dermatome. * If you see a zoster involving the ear. associated with lymphoproliferative diseases. Strep can travel extremely fast. then take them off antibiotics. It causes an extremely itchy bumpy area. * If there is a question. * Syphilis starts with a chancre (primary). from ankle to thigh in a single day. or kidney stone. Mark with pen to determine if treatment is working or if cellulitis extending. vertigo. It can be seen in other areas including the eye. many types. * Warts caused by human papilloma virus. Oral herpes can be brought out by sun as well. sarcoptes scabeii. you need to do a dark field exam of the chancre looking for spirochetes. It may be difficult to distinguish at the bedside from TEN because you see the skin sloughing off. and the interdigital webs of the hands. see oval salmon-colored patches over the body with palms and soles involved. increased protein. such as penis and scrotum. Patient may present to physician thinking they’re having a heart attack. such as cold sores. If you culture or Gram-stain skin. Often we cannot do a culture so treat for what you think it is (staph or strep). Petechia are non-blanching purple areas of the skin. Can be caused by a mixed infection or a strep infection. decreased glucose. -------------------------------------------------------------------------------------------------------------------------------------------Viral Skin Infections * Herpes is a viral infection that classically involves the mouth or genitalia. like staph bacteremia. facial palsy. They can get large purpuric areas with very minor trauma. Not everything that is purpuric is not a major infection. DO NOT DISTRIBUTE . * Treatment for SSS syndrome is anti-staph antibiotics. especially areola.Study Notes – Internal Medicine James Lamberg 28Jul2010 * Exfoliatin toxin causes skin to exfoliate. Only an average of 11 mites on entire body. axilla often involved. * Do Gram-stain of CSF looking for organisms. You need to scrap a spot and look for eggs. But we must treat quickly. * Cellulitis usually caused by staph or beta-hemolytic strep. Here in SSS syndrome. tender plaque. * Clinically you see groups of blisters on a red base. * HIV-positive patients can quickly develop tertiary syphilis with CNS changes. Senile purpura is seen in elderly patients with fragile blood vessels and connective tissue.46 - . treponema pallidum. mostly because those are the common areas of inoculation. The lesions have a smudges look and given time they will become vesicular and necrotic with a slate-gray center. This means there is hematogenous spread. Generally zoster begins with pain. the blood test should be positive. * Say you see many groups of blisters on a red base. think meningococcemia. * You may not see signs of meningeal irritation. The first case of a cold sore for a patient can be extremely angry if they have no immunity to it. If you see fever and rash. or sciatica. Generally it starts with a cellulitis and quickly the organisms go deep and make it to fascial planes. you won’t see anything because the staph is at a distant site and you’re getting the result of the toxin.
lymphoproliferative. * Dermal (intradermal) nevus is skin colored. Formed elements in blood cells like hemosiderin leave the dark spots.47 - . Melanomas start with melanoma in situ. diameter smaller than pencil eraser. benign. * Most common melanoma is superficial spreading type. * Basal cell carcinoma has pearly raised border with crust. Locations are the nasal labial folds. It appears and immediately invades. Other types are acral melanoma (hand. look at ABCD. but symmetry matters. the growth is out of control. Sometimes you see a pus bump.Study Notes – Internal Medicine James Lamberg 28Jul2010 -------------------------------------------------------------------------------------------------------------------------------------------Pigmented Lesions * Pigmented lesions come in all shapes and sizes. this is melanoma. Ask about family atopy. friction. meaning eczema simply on the basis of dryness. Bluish plaque like discoloration. Lymphocytes are destroying nevus. * Compound nevus. symmetric. Stage IV means all the way through to bone or muscle. They have a low metastatic rate. It never involves the palms. * Pityriasis rosea looks like secondary syphilis. Get a VDRL to rule-out syphilis also. rarely the palms. Sarcoma is a misnomer. -------------------------------------------------------------------------------------------------------------------------------------------Nail & Hair Disorders * Acute paronychia is an infection. Seen often in patients who get manicures. Skin gets so dry that is simply breaks down. eyebrows. If we can find them and treat quickly. Melanomas are asymmetrical and irregular. is a benign lesion with the melanocytes found at junction (epidermis/dermis). symmetric. Can turn into squamous cell carcinomas. Some of the nevocytes are at DE junction and some down into dermis. * Stasis dermatitis begins with venous insufficiency. irregular color. you see well demarcated rash only at location of problem (e.g. * 75% of squamous cell carcinomas on the skin are sun-induced. * Nevus with irregular border. Usually involves the knees and elbows. moisture from incontinence (urinary or fecal). specifically to staph. * Halo nevus is a symmetrical halo of lightness around a nevus. border. sheering forces (slipping down in bed). * Greasy stuck-on appearance are seborrheic keratoses. not well understood. It classically begins with a herald patch. and eczema. we can cure the patient in most cases. * Contact dermatitis from irritation or from allergic contact dermatitis. around ears. sometimes just red and tender. Diagnosis with biopsy. 70%. and III (mets). Keep in mind symmetry. This has an in situ phase lasing 6months to a year. * Treat by removing things that cause allergy. The exception is squamous cell carcinoma of the mucosa (lip) where there is a metastatic rate 10-20%. with red itchy patches in the flexures. They have lots of IgE in system. 15% of melanomas. overgrowth of top layer of skin. in the area around the nail. chemotherapy) and elderly (Mediterranean). sometimes the scalp. Next most common is nodular. * Eczema (dermatitis) can be asteatotic. Benign pigmented lesions tend to be symmetric. feet) with high mortality and lentigo malignant type seen on the sun exposed areas of elderly people and has good prognosis. This is benign. Decubitus ulcers caused by pressure. * Nodular melanoma may be more symmetrical than others. Skin can be thickened from scratching. Patients will have asthma. * Kaposi sarcoma seen in immunosuppressed population (AIDS. II (lymph). hay fever. but it is still irregular. Generally culture but always cover for DO NOT DISTRIBUTE . * Stages are I (skin). broken blood vessel on it possibly. Stage III is full-thickness skin breakdown but not to fascia. Stage I is non-blanching redness. Should be removed. * Atopic (allergic) eczema is usually seen in atopic families. Can cause nail changes (pits) and generally nail dystrophy (onycholysis). * Decubitus ulcers are defined in stages. * A junction lesion. benign. probably a neoplasm of epithelial cells likely lymphatic and small blood vessels. benign. * Actinic keratoses refers to an area of the skin which is scaly and caused by sun (sun exposed area). where it is only present at the epidermis. Prognosis is based on level of depth of invasion. oval slightly scaly salmon-colored patches over the body. So they react in an expected way to the staph that is on our skin. * Seborrheic eczema is a chronic condition with redness and scaling in classic locations. symmetrical. usually staph. poison ivy in linear blisters). They are precancerous. -------------------------------------------------------------------------------------------------------------------------------------------Papulosquamous (Scaly) Eruptions * Psoriasis is silvery scale on a red base. around 1%. rubbing. Generally do not metastasize. most common of all cancers. Stage II is very superficial breakdown. but the majority of patients do not develop cancer. Once a malignant pigmented lesion has occurred. scalp. If it presents at this stage without dermis involvement there is 100% cure with proper excision. Is this lesion symmetrical? Yea. In allergic contact dermatitis. color. Protein surrounds the vessels causing fibrin cuffs and preventing oxygen exchange so tissue becomes hypoxic and breaks down.
The lower part near the GE junction is columnar epithelium. it grows with the patients. Treat quickly because if swelling is great enough you can impair the blood supply to the distal tip of the finger. drain. It depends on where the cyst originates from. Tophi is sodium urate crystals deposited in the skin. -------------------------------------------------------------------------------------------------------------------------------------------Kaplan Videos (2001) – Gastroenterology with Dr. * Traction alopecia comes from chronic pulling of the hair so much so that the roots are destroyed. * Esophagus is made of smooth muscle except for the very top where there is some skeletal muscle. * Cavernous hemangioma appears in infancy and persists. Either way. Food travels down to the stomach at the gastroesophageal junction. * Acrochordons (skin tags) are benign and not associated with internal malignancy or anything else. They involute each year such that by the time the child is 9. * Clubbing can be seen in cyanotic heart disease as well. where the lower esophageal sphincter (LES) exists. could be a collection of mucopolysaccharides (benign and we drain) or a herniation of a joint sac. * Clubbing refers to a distal bulbous enlargement of the finger tip. * Disease of smooth muscle. Alopecia areata totalis covers all the hair in the head. Uric acid begins to deposit in the joint. generally appear early in life and enlarge during first year of life. capillary and cavernous. treat with antibiotics. such as emphysema. Could be a personal or familial tendency. * 90% of cysts on scalp are pilar cysts but you really can’t tell until you remove them. So decompress. causing joint pain. They are benign. * Hypertrophic osteoarthropathy looks like clubbing except there is tenderness at the distal fingers. * Hemangiomas are benign collections of blood vessels. This is completely benign. Seen more frequently in obese patients possibly more frequently in diabetics.Study Notes – Internal Medicine James Lamberg 28Jul2010 staph. By the end of the first year they generally stop enlarging and involute. It can also involve the nails. It is due to deeper dermal vessels. Often begins in 20s-30s and continues throughout life. tuberculosis. like scleroderma. * Androgenetic alopecia is male-pattern or female-pattern baldness. Capillary hemangiomas also called strawberry hemangiomas. skin epithelium or hair follicle epithelium invaginates under the skin and makes a pocket. * Digital mucus cyst are soft. with nail dystrophy. If there is no punctum connecting it to the surface. * Telogen effluvium seen after patient goes through tremendous physiologic stress. It is sometimes seen in a familial setting but most often in a patient with chronic lung problems. -------------------------------------------------------------------------------------------------------------------------------------------Benign Skin Growths * Gout is caused by chronic elevated uric acid levels. * Does food travel down the esophagus by gravity? No. the new hair pushes out the old hairs and there can be an enormous amount of hair loss. but there will be a few months of hair loss. soak. but gravity does play a role. * Food travels down the esophagus by ordered (sequential) peristalsis. Associated with lung carcinoma. The history makes the diagnosis here. Either way. The UES and LES will be at high resting pressure then DO NOT DISTRIBUTE . The most common types of cancers of the gastrointestinal tract are adenocarcinomas. These hairs will grow back. so anal cancer would be squamous cell carcinoma. Seen in patients who wear tight braids or tight pulling. Disease such as muscular dystrophies that affect skeletal muscle could cause disturbances in the upper esophagus. So all the areas of the esophagus are at low pressure at rest then higher pressure when moving food. The body is stressed so it is shutting off non-essential functions like hair growth. sometimes many of the hairs will all go into a resting phase (telogen). It is believed to be an autoimmune type of disease but poorly understood. This is a permanent scaring alopecia. so don’t do it. 90% have completely disappeared. That is why staying sitting up after eating is a lifestyle modification for GERD. what is the diagnosis or how do you make the diagnosis? * Hypopharynx empties food into the upper esophagus via the upper esophageal sphincter (UES). Also benign. Biopsy of this is difficult and causes lots of bleeding. universalis covers all the hair of the body. * Sebaceous cysts divided into epidermoid cyst and pilar (trichilemmal) cyst. surgery. That skin keeps making oil/sebum but is in a pocket. MD -------------------------------------------------------------------------------------------------------------------------------------------Gastroesophageal Reflux Disease (GERD) * Esophagus is a simple structure. no need to worry. When new hairs begin to grow in a month or two. delivery of a baby.48 - . Asher Kornbluth. * Alopecia areata is oval or round patches of complete hair loss. There will be periosteal thickening of the distal phalanx and often gynecomastia. if from dermis it is epidermoid and if hair follicle then pilar cyst. * Most of the esophagus is squamous epithelium. all you see is a nodule. Over time it will deposit in skin giving chalky subcutaneous masses called tophi. bronchiectasis. Given symptoms. affect the esophagus greatly. There are two types. There is squamous epithelium at the anus again. infection.
then you should start treating the patient. He is given sublingual nitroglycerin and notes his chest pain worsens. * Gold standard is not endoscopy. The magnesium is not absorbed and causes osmotic diarrhea. Over time they will have trouble with soft foods then liquids. These drugs inhibit the parietal cell from secreting acid.49 - . Primary peristalsis is voluntary and secondary peristalsis is involuntary. hoarseness. Most patients with GERD do not get Barrett esophagus and most patients with Barrett esophagus do not get adenocarcinoma.g. His physical exam is unremarkable. You see these pressure spikes and dips on esophageal manometry. * Barrett esophagus does not hurt and you can’t see it on an x-ray or barium swallow. rabeprazole. loss of peristalsis near the junction. * 24h pH monitoring is the gold standard for diagnosing GERD. You can only diagnose it with endoscopy with biopsy. pain with speaking. The endoscopist can suspect Barrett because the color of Barrett mucosa is more red than the surrounding mucosa. They can swallow liquids and soft foods. allergy). Remember that common things happen commonly. GERD. not necessarily correlating to how bad the symptoms are. * GERD medication for mild symptoms with longer relief is the H2-receptor antagonists. but solid foods are difficult (mechanical dysphagia). Tell patient not to lay down within an hour or so of eating. * Most common causes of chronic cough are: post-nasal drip (e. * 32yo man comes to the ED for substernal chest pain of two hours duration. * Chronic acid exposure at the lower esophagus. Nearly all of these are available over the counter because they are generally safe DO NOT DISTRIBUTE . the reflux is neutral (non-acidic) so causes no major damage. That does not mean all patients should get this. When food hits the upper esophagus you get secondary peristalsis.Study Notes – Internal Medicine James Lamberg 28Jul2010 going to low pressure to allow food to pass. So even if you LES is wide open and you reflux all day. * GERD medication for mild symptoms would be antacids if sporadic like magnesium hydroxide or calcium carbonate. Theoretically the patient will stop making all their acid and become achlorhydric. Other causes include decreased saliva in smokers as saliva buffers acid. or fatty foods because they opens the LES. chocolate. Examples are cimetidine. Single best drugs are proton pump inhibitors (PPI) like omeprazole. or x-ray because those do not show you that acid is coming back up in waves. * Barrett esophagus can lead to adenocarcinoma. * Nocturnal means it awakes the patient at night. famotidine. * Your only chance at cure for any GI tract cancer is resection. He says that he sometimes gets the pain while lying in bed at night. That is very suggestive that the symptoms are from GERD. Avoid foods like caffeine. He is otherwise free of symptoms except a non-productive cough the he has had for the past month or so. decreased smooth muscle function due to scleroderma. Aluminum gives you minimum stool (constipation). asthma. subxiphoid. cardiac is ruled out. * High grade dysplasia management is to confirm the biopsy report with a second expert pathologist because there is a fair amount of inter-observer variation. Patient wears a pack like a Holter monitor for that time. 1-2 years depending on dysplasia grade). The pain was probably burning. * Gastroesophageal reflux disease (GERD) is most commonly caused by LES laxity.g. this is a key symptom if associated with any disease. * Symptoms of GERD outside the esophagus include laryngitis. So acid-induced bronchospasm. chronic nonproductive cough. nocturnal wheezing or coughing when laying flat * Pulmonary symptoms of GERD are due to acid making its way all the way up and past the UES. esophagitis). lansoprazole. esomeprazole. * Diagnosis of GERD is made by history. You may even find adenocarcinoma once the entire esophagus is removed. Avoid cigarettes smoking because it dilates the LES and decreases esophageal mucus. * Say patient has chest pain. ranitidine. * Primary peristalsis begins when you swallow something. Antacids do not eliminate the acid. Histologically it looks like small intestine cells. Makes you Go. “A chance to cut is a chance to cure. Side effect of magnesium hydroxide antacids is diarrhea. barium swallow. do esophageal resection because it is very likely to develop cancer.g. * GERD treatment after lifestyle is medication. Barrett esophagus is metaplasia from squamous to columnar mucosa at the distal esophagus. * Low grade dysplasia management is treat GERD aggressively for a few months then re-biopsy. Once confirmed. What do you think is the most likely diagnosis? GERD. Barrett patients should undergo surveillance endoscopy at some interval (e. The test that does do that is 24h pH monitor via catheter through nose that has pressure transducers along the catheter and a pH probe at the end. radiating up. nizatidine. also known as inappropriate relaxation of the LES at rest. pantoprazole. Patient has longstanding GERD and presents with dysphagia. then refluxing into the lungs and causing a chemical irritation of the bronchi. However. but redness is non-specific (e. which is why we are about this finding. they buffer it. You do 24h pH monitor and it shows distal to mid esophagus pH is 2-3 during the 24 hour period. * Mnemonic: MG. alcohol. * Peptic stricture is a smooth tapering of the lower esophagus due to chronic GERD.” * Most esophageal cancers are not cured because by the time the patient presents with dysphagia the cancer has already advanced past the wall of the esophagus. * GERD treatment begins with non-invasive lifestyle modification. can lead to Barrett esophagus.
In scleroderma. The most common cause is reflux. Or another example say the patient is symptomatic and no longer wants to take medications. The beak is the contracted LES. If not tight enough. She has occasional difficulty swallowing liquids. That pump is blocked by PPIs. So inhibition will result in contraction. She has had the problem for over a year and has trouble with solid foods. * You need esophageal manometry to diagnose the particular kind of motility problem. then PPIs. * Metoclopramide inhibits dopamine. * Nitrates and calcium channel blockers are smooth muscle relaxants. Barium swallow will slow a DO NOT DISTRIBUTE . increasing the chance of polymorphic ventricular tachycardia. esophageal dysmotility. added metoclopramide and the patient still has symptoms. Lack of dopamine causes Parkinson-like symptoms. * Limited systemic sclerosis is also known as CREST syndrome: calcinosis. Drugs like cimetidine or azithromycin could potentiate cisapride. barium swallow) as being the first step. You also see inappropriate contraction of the LES that does not relax. * Manometry of diffuse esophageal spasm would show diffuse disordered peristalsis. When you do an upper GI series (i. Say you do a manometry and see flat-line with no spikes and the LES does not relax. the fundus is wrapped around the LES so that the LES has a sleeve tightening it. sclerodactyly (thick tight skin). which is a bad price to paid for heartburn. Can be done laparoscopically. * Nissen fundoplication is usually done laparoscopically. Raynaud phenomenon. He continues to have the pain. Why don’t we use metoclopramide as primary treatment? Because dopamine receptors are also found in the brain. but this does not work very well long-term. thus metoclopramide can tighten the LES. In this surgery. Surgery should be considered after no relief from maximal medical therapy. The drug was pulled due to a fair number of sudden deaths. Another option is to inject the area near the LES with botulism toxin because that poisons the acetylcholine. What is the next step in the evaluation of this patient? * Dysphagia means difficulty swallowing. There are some others that cause chest pain because the esophagus goes into tight spasm. telangiectases.g. but the major side effect is torsades de pointes due to prolonged QT. Give large dose PPIs. Maybe there is a cancer near the esophagus or there is a stricture. such as tardive dyskinesia. Metoclopramide will not help tighten the LES because the LES is now replaced with collagen. You cannot make the diagnosis of achalasia without an esophageal motility study. and inhibits CYP450 so be careful with drugs like warfarin and theophylline. but there is also no motility to wash the acid back down so the reflux can be very severe. * There is no good treatment here other than treating reflux as aggressively as possible. The next step is surgery. * With achalasia. Whatever stimulates the parietal cell. Acetylcholine keeps LES shut at rest. it increases gastric motility and emptying so acid is put further downstream. the final pathway to acid secretion is via the hydrogen-potassium ATPase pump. Definitive procedure is a myotemy. the patient will have dysphagia. So also do an endoscopy with biopsy when you see achalasia. It tightens the LES by simulating cholinergic receptors. then went to H2-blockers. H2-blocking reduces but does not eliminate acid because parietal cells are stimulated by other things.e. Dopamine at the LES causes relaxation. This is classic for scleroderma. Cisapride was very effective. barium swallow). * Say you tried lifestyle modifications. * 32yo woman with motility dysphagia. Odynophagia means pain with swallowing. If the wrap is too tight. The symptoms have not worsened at all over this period and the physical examination is unremarkable. some confusion in the elderly. * If there is progressive narrowing then suspect mechanical dysphagia. go straight to the PPI medications.Study Notes – Internal Medicine James Lamberg 28Jul2010 and are effective for most people. Esophageal manometry shows flat-line of no peristalsis but the LES is also flat-line (low pressure). You do a 24h pH monitor and the pH is still 2 or 3. Motility dysphagia has symptoms that do not depend on the size of the food. The LES is open so they get reflux. * With most dysphagia. * 30yo man with mid-chest pain has had several negative cardiac workups. the patient still has reflux. This is achalasia. you see a bird’s beak esophagus with barium. So a patient with chest pain who got worse with nitroglycerine we would suspect GERD once cardiac is ruled-out. PPIs are also available over the counter more recently. Dysphagia * 32yo woman with no past medical history comes to your office for evaluation of difficulty swallowing foods. * Histamine binds to parietal cells and stimulates the release of acid. there is invasion of the neural plexus that causes contraction. * Achalasia is rare and even less common is pseudo-achalasia where you see the bird’s beak but in reality the cause is a gastric carcinoma wrapping around the LES. * Treatment of achalasia is usually be pneumatic (balloon) dilation at the LES to tear the muscle fibers. More so. so they would relax the LES. a Nissen fundoplication. The cause is likely esophageal motility problem. So there is no peristaltic waves in the esophagus. think of an x-ray (e. * Cimetidine can cause gynecomastia in men. the esophageal smooth muscle is replaced with collagen and LES replaced with collagen.50 - . * Cisapride is no longer available. * If you do endoscopy and see erosive esophagitis. the surgeon cuts the muscle fibers of the LES so it is permanently opened.
The barium swallow is done first to help determine if you can get an endoscope through since there is a risk of perforation. He has had no prior episodes except nine months ago he had a single similar episode that gradually resolved over several hours. He notices people tend to keep their distance from him because of this. if you find the Virchow node you assume gastrointestinal cancer. the most common being colon cancer in the United States. Barium x-ray would show a ring or band near the LES. Work hard to rule-out cardiac causes of chest pain before you jump to the motility work-up. Squamous cancers along with head/neck cancers are associated with chronic alcohol use and smoking. These peri-umbilical nodes are called Sister Mary Joseph nodules. But most likely Zenker diverticulum. He has a medical history of significant reflux esophagitis for 15yrs and a 40pack-year smoking history. * So 62yo guy with dysphagia. * 62yo man comes for evaluation of progressive difficulty swallowing solids and recently semi-solids for four months. * Most patients with esophageal carcinoma will give a history of smoking and/or alcohol use. so they also get a surgical cricopharyngotomy (cricopharyngeal myotomy) of the UES. Think cancer until proven otherwise. He coughed up the chicken teriyaki that he ate two days earlier. But. more commonly seen in an older patient and associated with coughing and gurgling as soon as they start eating then spit it back up.Study Notes – Internal Medicine James Lamberg 28Jul2010 corkscrew esophagus as there is diffuse non-ordered peristalsis. no diagnostic test needed to tell us this. * There is no medical treatment for Zenker diverticulum. but it doesn’t really matter because surgery is the only hope for a cure. The gut lymphatics drain through the left supraclavicular node. So what tests do you do? There is some controversy. This past weekend a most disturbing event occurred while he was watching a football game. you can jump to the endoscopy to directly visualize the ring. * Primary treatment for any esophageal cancer is surgery. squamous carcinoma since we are at the top of the esophagus. you find a 1. but the history is not progressive it is episodic. * Treatment via endoscopy would be removal of stuck food or carefully pushing the food through the soft ring. Barium x-ray would show an upper esophageal ring. * Zenker diverticulum most commonly at upper esophagus. Then do the endoscope with biopsy. almost always adenocarcinoma. major weight loss. He has had a 20lb weight loss. Other options include pneumatic dilation. * 75yo man comes to see you because he thinks he has bad breath. Esophageal Cancer * Plummer-Vinson syndrome signs include upper esophageal web. but treatment is the same (surgery). * Nodules in or around the umbilicus are also highly suggestive of gastrointestinal cancer. iron deficiency anemia.51 - . * 40yo man presents to the ED after going to dinner. * Virchow node is not common. Pushing the food can break the ring too. * Treatment of diffuse esophageal spasm is nitrates or calcium channel blockers to relax the smooth muscle. The Schatzki ring is always found just above the LES. but that is adjunctive therapy. This often occurs in the setting of a tight UES. The story is William Mayo (Mayo clinic) was a surgeon at the beginning of the 20th century. * Nobody died of a little bit of esophageal spasm. treatment is surgical diverticulectomy. With these think of a gut cancer. Schatzki ring thought to be due to chronic acid exposure. On physical exam. also known as steakhouse syndrome.5cm left supraclavicular lymph node (Virchow node) but otherwise exam is normal. What is the next step in the evaluation of this patient? * Can this be achalasia? Yes it can be. It is a risk factor for esophageal cancer. meaning of all those that have gastrointestinal cancer only a few will have the Virchow node. and angular cheilosis. but go with barium esophagram first. Physical exam is normal. If the history is classis though. * Some evidence that squamous carcinoma responds to chemotherapy and radiation. Mayo’s patients. Thus. He complains of severe chest pain and feeling that food is stuck in the mid-chest. Food can sit there for some time but typical history is coughing food back up at the time of eating. The cancer can be anywhere in the esophagus and it usually takes an irregular ulcerated pattern. Think Plummer-Vinson when you see a low Hct and low MCV with upper esophageal issues. Since then he has had no heartburn or weight loss. most things get through until you hit the critical diameter like a large piece of steak that does not get through. He has esophageal cancer. * Episodic mechanical dysphagia (large bolus of food) should suggest a Schatzki ring. The term nutcracker esophagus is used because the manometry peristaltic wave pressure can be so high it is said they can crack a nut. Virchow node. DO NOT DISTRIBUTE . Biopsy important near the LES to distinguish squamous carcinoma from adenocarcinoma. We don’t know if this patient has squamous cell carcinoma or adenocarcinoma. * Diagnostic test is barium esophagram showing pocket. He claims to brush his teeth every night. so not a fibrous piece of tissue. may show an apple-core lesion on barium swallow. The caliber or width of the ring is variable and in general it is soft mucosa. Once in a while she would feel the nodules in the umbilicus. All the Mayo nurses at the time were nuns and Sister Mary Joseph did the surgery prep for Dr. Of course you do the diagnostic tests though prior to surgery.
* Ulcer seen in esophagus and you want to determine what kind. Vagotomy and antrectomy are not common anymore due to the prevalence of effective ulcer mediations. * Esophagitis in HIV patient think endoscopy with biopsy. and HIV-caused ulcer (least common) all of which are indistinguishable from each other. in this particular incidence. * Histamine stimulates the parietal cell and acetylcholine as well. * Treatment for HSV esophagitis is acyclovir. prednisone for an immunocompromised patient with an infection? Yes. Stomach makes pepsin. a protease.Study Notes – Internal Medicine James Lamberg 28Jul2010 * Caustic ingestion especially with lye can lead to strictures. It is a complete horizontal full-thickness tear of the esophagus casing esophageal separation. This is life-threatening. gastrin) it does not matter because the whole cell output is blocked. a longitudinal mucosal tear (not full thickness). You’d lose parietal cells with a sub-total gastrectomy or patient has a large gastric tumor that gets removed. can be just dysphagia though. HSV usually shows small discrete ulcers without plaques. Stomach also secretes gastrin. If symptoms relieve in 7 days. What is the next best test? Endoscopy. * Water and bicarbonate secreted in the stomach. arriving at parietal cells in the body of the stomach and stimulating the hydrogen-potassium ATPase pump whereby hydrogen gets secreted into the lumen of the stomach. You won’t see infectious agents on barium x-ray. Parietal cell also secrets intrinsic factor for vitamin B12 absorption. * Intrinsic factor from parietal cells is essential for absorption of dietary B12. some need endoscopic treatment. * Mallory-Weiss diagnosis is made by endoscopy seeing the lacerations.52 - . * Thrush looks the same in the esophagus. Esophagitis * The most common cause of esophagitis is GERD. * With the exception of the HIV patient. rarely steroids. * Common symptom of esophagitis is odynophagia. DO NOT DISTRIBUTE . Gastrin is secreted and travels through body in bloodstream. There is no endoscopic determination that can be made visually to determine what kind of virus. Types that occur are CMV. Wait. if the patient has esophageal symptoms and thrush on their tongue it is fair to say the patient has esophageal thrush (candidiasis). Intrinsic factor links with B12 and get absorbed in the terminal ileum. Give prednisone for a week and if symptoms disappear you have confirmatory evidence that it was HIV-induced ulcers. Next most common are infectious agents. or famciclovir. * Pernicious anemia is due to loss of parietal cells and thus loss of intrinsic factor. * Biopsy will show cytomegalic cells and/or owl’s eye inclusions (CMV) or ground glass cells and/or Cowdry type A bodies (HSV). You can scrape the plaques off and put them on a slide (KOH prep) to see budding forms and hyphae. * Treatment for CMV esophagitis is ganciclovir or foscarnet. You can remove the stomach and do just fine with proteins though because the pancreas creates plenty of proteases. Rather than put the patient through endoscopy you can treat them with fluconazole. The Gcells in the antrum secrete gastrin so removing the antrum (antrectomy) would eliminate another stimulus for acid secretion. so HIV. Pernicious Anemia * Chief role of the stomach is to grind food as only several millimeters can get through the pyrosis. * Most Mallory-Weiss tears resolve on their own. * The benefit of PPIs is that no matter what the stimulation to the parietal cell (histamine. which are the natural defenses against HCl. Virology can show which grows out but viral cultures are unreliable. * Boerhaave syndrome is also caused by retching and is much more rare. white cottage cheese-like plaques. acetylcholine. Endoscopist can do various techniques to stop the bleeding at that point if required. They keep vomiting and red fluid starts coming up (blood). * Medical student goes out to celebrate passing USMLE Step 2 and drinks too much then begins to vomit up the steak that they ate. It is not from the HIV as the initial insult but due to the inflammation that the HIV causes. However. * Immunocompromise increases risk for infectious agents. * Say the patient has no thrush or had thrush but still has esophageal symptoms a week later. This is a Mallory-Weiss tear. chemotherapy. They keep vomiting and bile starts to come up (stomach empty). a stimulant from antral cells. HSV. candida is usually in the upper third of the esophagus with small nodules. Treat with fluconazole. you know the patient had candidiasis. Over time the strictures can degenerate into squamous cell carcinoma. There are several types of infectious ulcers that can cause symptoms. * Acetylcholine comes from nerves so a surgical vagotomy would eliminate one stimulus for acid secretion. Intrinsic factor is not needed for subcutaneous B12 injections because that does not absorb via the GI tract. CMV usually shows severe inflammation with large ulcers. leading to megaloblastic anemia. valacyclovir. so it plays a minor role in digestion of proteins. * We have H2 blockers but no real drugs in clinical practice to block gastrin or acetylcholine at the parietal cell. * Treatment for HIV-induced ulcer (diagnosis of exclusion) is prednisone. Anti-cholinergic drugs have poor side effects like dryness and urinary retention.
* COX-2 metabolites are leukotrienes. is not very helpful. do endoscopy with biopsy of the antrum and the pathologist will find H. but least expensive test. women can buy these medications to abort early in pregnancy (less efficacious later in pregnancy). amoxicillin. and has a number of actions leading to ulcer production (e. * Mnemonic: MTB. cytotoxic. * Gastrinoma is a tumor comprised of gastrin cells. * CLO test is taking biopsy tissue from antrum and putting it in yellow gel. pylori was once named campylobacter-like organism. Called CLO because H. Non-specific cyclooxygenase (COX) inhibition is seen with older NSAIDs like ibuprofen. azithromycin. Could be folate or B12. Zollinger-Ellison syndrome. pylori has many regimens. in non-ICU patients who are not taking steroids or drinking alcohol. is infection with Helicobacter pylori. * Intrinsic factor from parietal cells goes back and shuts down gastrin. boring pain (meaning it feels like it is going to bore through you). and asprin. * Pain that is better with eating and then gets worse. Bismuth also has bactericidal effects. COX-2 inhibitors include celecoxib and acetaminophen. * There it lots of overlap between gastric and duodenal ulcer symptoms. * H. ulcers are most likely due to NSAIDs. You do endoscopy and see ulcers. creates an alkaline environment around itself to protect from HCl. with or without nausea. patient on PPI might be 80-100. Methotrexate is used to kill the fetus and misoprostol is used to evacuate the fetus. repeated ulcers). * If patients has rheumatoid arthritis and ulcers. tetracycline. we use PPIs.Study Notes – Internal Medicine James Lamberg 28Jul2010 * Autoimmune disease (more common in women) can cause megaloblastic anemia later in life via autoimmune destruction of the intrinsic factor. In countries where abortion is legal. make tummy better. Ulcers * Typical symptoms of any ulcer is epigastric pain. are important in the cytoprotection of the stomach. which was the cause of rofecoxib being pulled off the market in 2004. gastric or duodenal. * Bactericidal antibiotics for H. look for anti-parietal cell antibodies and anti-intrinsic factor antibodies. * Non-invasive tests for H. Classic symptom is nocturnal epigastric pain that wakes someone from sleep. stimulates meal-induced gastrin). tetracycline. Prostaglandins increase intestinal motility and uterine motility. Least accurate test is blood IgG looking for antibody. usually outside the stomach. clarithromycin. Although there is come controversy on acetaminophen as it does not exhibit anti-inflammatory properties. omeprazole. you’d want to go with the COX-2 inhibitors. * Misoprostol is an analog of prostaglandin. So being more specific with COX2 blocking will help relieve aches and pains but not block the prostaglandins that are important for gastric protection. pylori on the surface of the antrum. If patient has NSAID-induced ulcer. * Treatment for H. Normal is < 50 blood gastrin. which is very accurate. So every patient with an ulcer should be tested for H. bleeding (could ulcerate into a vessel). then stop NSAIDs and try to make the ulcers better. does not differentiate current from past infection. would also show sky high blood gastrin levels. the gastrin goes high to 1000 range. * NSAIDs come in COX1 and COX2. gastric outlet obstruction symptoms (chronic scaring. this is a black box warning. * If you treat an ulcer but not H. pylori. * With H. * Another regimen is MOC. penetrating (pancreatitis as ulcer bores into back). a negative feedback loop. So with no acid. Trying to distinguish the type of ulcer based on getting better or worse with food. It is specifically designed to defeat the problem of NSAIDs. * Neutrophils in pernicious anemia will be hypersegmented. The gastrin-secreting cells are autonomous (not shut off by acid section). sometimes three. pylori negative. naproxen. It is not an invasive organism. Proton pump inhibitors are useful too. bismuth. * The vast majority of community acquired ulcers. Always use at least two antibiotics. DO NOT DISTRIBUTE . COX-1 metabolites. metronidazole. relation to food (might be improved or worsened). metronidazole. gnawing pain. To determine if you treated the patient accurately you can check a repeat breath test or stool antigen test. pylori. Mnemonic for -coxib drugs to remember COX2 is “-cox” and “b” for 2nd letter in alphabet. there is over a 90% chance that the patient will develop another ulcer. pylori include breath tests to measure for exhaled urease.g.53 - . remember you never use a single drug because resistance becomes problematic very quickly. If asked what drug will reconstitute prostaglandin activity. pylori is a Gram-negative organism that lives in the antrum of the stomach in the mucus bicarbonate layer. Side effects are diarrhea and abdominal cramping. They maintain good blood flow to the stomach and tight gap junctions. and some label it as COX-3 (but COX-3 does not have anti-pyretic properties). * Never give misoprostol to pregnant women or even women of childbearing years. namely prostaglandins and prostacyclin. clarithromycin. pylori include metronidazole. then pick misoprostol. perforation (surgical emergency). think peptic ulcer disease. * Biopsy of patient with pernicious anemia would show atrophic gastritis. It secretes urease. Misoprostol is part of a home abortion kit. Urease will turn the yellow gel to pink. COX-2 specific medications have been association with vascular events. * Ulcer complications include pain. Say you had a positive biopsy or breath test and you treat the patient.
use COX-2 in future. * NSAID-induced ulcers treated with PPIs. With gastrinoma there is no feedback inhibition so serum gastrin is in the hundreds or thousands. If you give secretin IV and gastrin level increases. * Think gastrinoma when you see diarrhea with multiple ulcers. problem-specific treatment is misoprostol. Gastroparesis * The majority of gastroparesis cases are seen in diabetic patients. * There is damage to the neural innervation of the stomach. We do have a drug that suppresses acid so use that. * Cisapride no longer used due to increased QT interval leading to torsades de pointes. * Test to order is a serum gastrin level. do an imaging study like a CT scan looking for the tumor. Then when the insulin wears off. * Erythromycin is the next option because it stimulates motilin receptors. biopsy to determine if benign cause versus malignant cause like adenocarcinoma. * Treatment includes metoclopramide to improve gastric motility. but not to the 100s range with a PPI. * Most important thing to ask in a patient with an ulcer is does this patient have Helicobacter. usually Type 1 diabetes. peritoneal signs. they feel gassy and bloated. The goal of timing is to match when the carbohydrates are digested in the small bowel mucosa. Her past medical history includes peptic ulcer disease for many years that has been relatively resistant to medical treatment. secretin inhibits gastrin production so you see a fall in serum gastrin. 2 hours later when the regular insulin works the patient has a period of hypoglycemia. Some of the tumors can be microscopic and you can have metastatic Zollinger-Ellison syndrome rarely. the food hits the small bowel and the patient gets hyperglycemia. She has stopped all dairy and milk products for the past few months because another physician told her that her symptoms were caused by a lactase deficiency.Study Notes – Internal Medicine James Lamberg 28Jul2010 * Perforation would present as an acute abdomen. associated with gastric adenocarcinoma as well as gastric lymphoma. What is your next step in evaluation of this patient. think Zollinger-Ellison syndrome. She takes maximum doses of omeprazole daily along with famotidine and still has symptoms. feel progressively uncomfortable throughout the day. free air under the diaphragm. Gamma counter put over patient to see how long food sits in the stomach. Lab results are normal except for mild hypercalcemia. Wouldn’t omeprazole increase serum gastrin level? Yes. * Once high serum gastrin is confirmed by secretin stimulation test. Obstructing lesion would show scaring and inflammation from the ulcer on endoscopy. The motilin receptor in the stomach responsible for peristalsis gets activated because erythromycin simulates the motilin hormone. In normal people. there is always an association with DO NOT DISTRIBUTE . to confirm you are not dealing with a mechanical obstruction. then you inject secretin via IV. pneumoperitoneum on x-ray. Gastrinoma (Zollinger-Ellison Syndrome) * 42yo woman comes to your office with complaints of diarrhea for six months. * Gastrinoma tumors. take it out. 95% of cancers in the stomach are adenocarcinoma. There has been no improvement in symptoms. often microscopic. What would cause this? An autonomous constant drive to secrete gastrin. are usually found in the head of the pancreas or region of the common bile duct and usually not found in the stomach. Patient eats a meal mixed with nuclear chemical. which is important for peristalsis. * The diarrhea is due to the acid spilling out into the pancreatic area. or other ulcer problems * The patient still has ulcers even at maximal PPI therapy. * Secretin stimulation test is done by measuring baseline fasting gastrin level after stopping omeprazole. The diarrhea occurs throughout the day and she has not noticed blood or pus with the stools. * Look for other signs of neuropathy like autonomic dysfunction (orthostatic). may ultimately need to vomit to relieve the symptoms. * H. If the food just stays in your stomach for 8 hours. * What if you can’t take the tumor out? Do we have a drug that reduces gastrin? Not currently.54 - . Physical exam is unrevealing. whether x-ray or endoscopy. Side-effect is dopamine inhibition and therefore Parkinson-like symptoms like bradykinesia. about 5% are gastric lymphomas. Secretin is released by the small bowel to cut down acid production by causing water and bicarbonate production. * Test is nuclear gastric emptying scan. If you can find the tumor. a gastrinoma. causing hypercalcemia. pylori is present in patients with gastric ulcers and duodenal ulcers. Treat patient with multiple antibiotic regimen for about 14 days. * Why hypercalcemia? MEN-1 syndrome associated with parathyroid tumor. You have to do some test. * Antacids may be used in addition to the other medications for ulcer symptom relief. * Mucosa associated lymphoid tissue (MALT) is a localized lymphoma. bad history of ulcers. You would get a prolonged gastric emptying test with gastroparesis or a mechanical obstruction like a tumor pushing up against the gastric outlet. * Signs of gastroparesis are feeling full very quickly after eating. which inactivates the pancreatic enzymes and there is ineffective digestion. massive doses of PPIs. * This can be a particularly difficult problems for diabetics because they time their insulin doses with eating.
* By definition. enterocolitica is the most common contaminant of stored blood and can live at lower temperatures (e. Crohn is transmural through the full thickness of the bowel wall. is called a syndrome because there is nothing we can point to that looks inflamed or abnormal. radiation. pylori. * UC occurs over weeks to months. Bloody diarrhea for a few days is more likely to be infectious colitis. no anti-platelet action). usually presents as a younger women (teens. Sulfasalazine is sulfa connected to 5-ASA. 32yo woman visits due to problems with fertility. You want to see the whole colon so do a colonoscopy. * Acute terminal ileitis associated with Yersinia enterocolitica. If just the rectum. it is proctitis. IBS is not associated with any inflammatory signs or symptoms. or surgery. No fevers. anti-spasmotics for cramping pain. pylori treatment without chemotherapy. maybe altered sensitivity to pain sensation in the intestines. there is symmetric circumferential continuous disease for some portion of the colon. so anti-diarrheal agents if needed. admit for IV steroids. May occur with other syndromes that have vague symptoms like fibromyalgia or chronic fatigue syndrome. * Say patient is not improving with sulfasalazine or mesalamine. etc. negative stool studies will help rule out infectious agents. not guaiac positive (unless they have hemorrhoids from straining if constipated). no anemia of chronic disease. diarrhea. Side effects of sulfasalazine tend to come from the sulfa portion. Inflammatory Bowel Disease (IBD) * Inflammatory bowel disease (IBD) covers Crohn disease and ulcerative colitis (UC). 20s. refrigerator). showing cobblestone pattern. Crohn occurs in patches. specifically Ashkenazi Jews. Older patient for a few days it might be ischemic colitis causing bloody diarrhea. it is a stool packaging factor. * Patient gets endoscopy and lymphoid tissue is found in the stomach (MALT).55 - . * Irritable bowel syndrome (IBS) is far more common than any other bowel condition. whether it is sulfa intolerance with headaches. Another name for 5-ASA is mesalamine or mesalazine. * IBS treatment is to increase dietary fibers. no peritoneal signs. next step is steroids (oral or rectal). no organomegaly. 30s). aggressive doctors may use cyclosporin. or more commonly alternating diarrhea/constipation). The “nervous stomach” people get before big exams is sort of an irritable bowel symptom. pancolitis. If that fails. nausea. so a reversible side effect. which is always present in MALT. * Crohn disease can affect the colon but specifically there will be terminal ileum involvement. symptoms include combination of crampy abdominal pain associated with altered bowel habits (diarrhea. no matter DO NOT DISTRIBUTE . Although 5-ASA looks like aspirin. * Mesalamine can be given as an enema or suppository as well * Sulfasalazine. Sulfasalazine may be the cause. * IBS thought to be due to altered motility in the bowel. left sided colitis. blood counts are good. Once medical therapy fails. About a liter a day leaves the ileum and enters the cecum. no weight loss. higher incidence in Jewish particularly of Eastern European origin. * Treatment of UC is sulfasalazine and steroids. After stopping the medication sperm counts will return to normal. it has none of those effects (no anti-inflammatory outside the gut. More of a vague non-specific exam. These patients can sometimes be cured with plain H. Entire colon. * Crohn disease is also a chronic disease but unlike UC. UC affects the mucosal layer only. If colon is ulcerated and inflamed. So look for terminal ileum inflammation. Biopsy will show mucosal inflammation. look for bowel irritants like food and stress.Study Notes – Internal Medicine James Lamberg 28Jul2010 Helicobacter. bloody diarrhea. some weight loss. no elevated sedimentation rate. it cannot do its job so you get diarrhea and blood. Treatment is antibiotics. constipation. * In IBS. skip lesions. vomiting. * Job of the colon is to absorb water. stool softeners or laxatives as needed. so colon absorbs about 85% of the water giving you 150mL of liquid in the stool. Yersinia is siderophilic (iron-loving) so patients with hereditary hemochromatosis are more susceptible. or rare photosensitivity. * Treatment for IBS is symptomatic as well. no night sweats. What do you do? Answer is treat H. showing lead pipe pattern. no mucus or pus in stool.g. or rare hemolytic anemia. * Any ethnic group can have Crohn disease. * Ulcerative colitis starts at the distal rectum right above the anus in the columnar mucosa. Diarrhea can be bloody but more typically is non-bloody diarrhea. affects the sperm count and sperm motility. terminal ileitis. the patient will not have focal findings. Y. the anus is not involved. So you have ruled out inflammatory diseases when you diagnose IBS. Disease to the splenic flexure. If that fails. * UC never involves the ileum and is always continuous. Many patients with Crohn disease will have a relative with the disease. * Test for UC can be done on the first visit via a flexible sigmoidoscopy. If rectum and sigmoid. Her medical history is negative but he has ulcerative colitis. no nocturnal diarrhea. protosigmoiditis. Full body workup for lymphoma is negative. * Crohn disease symptoms are abdominal pain usually RLQ. but not mesalamine. Rule out infectious etiology before labeling them with this life-long disease.
emerging to the perianal area or buttocks draining mucus. * Diagnostic test for Crohn disease is upper GI series with small bowel follow through. after 10 years of UC disease in the colon the patient requires colonoscopy surveillance to see if the patient is developing dysplasia. Unlike in UC. use mesalamine alone because it is generally released higher up in the intestinal tract. foul smelling stools. such as a toxin. * Perianal fistulas can occur in Crohn disease. ulceration. Treatment of giardia is metronidazole. pyoderma gangrenosum). give IV infliximab. * Failed medical therapy in Crohn should go to surgery. Surgery also for complications of Crohn like progressive small bowel obstruction or perforation or bad fistulizing disease with abscesses. However. Side effect of metronidazole is upper GI discomfort (nausea). acute onset. Side effects include a lupus-like drug reaction with antihistone antibodies. serum creatinine is 2. iritis). numbness/tingling due to peripheral neuropathy. Treat with fluids.g. Mnemonic: infliximab inflicts pain on TNF. particularly UC in the colon. * Campylobacter jejuni is one of the most common causes of enteritis. treat with quinolones or erythromycin. Enterotoxic E. It is a monoclonal antibody (-mab) against tumor necrosis factor (TNF-alpha). Vibrio cholera) watery diarrhea without mucus or pus or blood or fever. coli. disulfiram-like reaction with alcohol causing bad nausea/vomiting (rare but serious). headaches. remove the entire colon. * Extra-intestinal manifestations of IBD include arthritis (e. Do an upper GI series with barium then give extra barium to get to distal ileum. entamoeba histolytica. DO NOT DISTRIBUTE . VIPoma (vasoactive intestinal peptide). coli can respond to antibiotics like TMP-SMX or quinolones. hematocrit is at 19%. pus.Study Notes – Internal Medicine James Lamberg 28Jul2010 how much of the colon is affected by UC. do rectal parasite testing looking for ova or protozoa. Low grade dysplasia is treated by treating UC and seeing if it goes away. Infliximab not needed every day. and/or stool. and primary sclerosing cholangitis (sclerosis/fibrosis of the bile duct. Inflammation can occur in anal crypts and burrow through the soft tissues. campylobacter) bloody diarrhea with fecal leukocytes and fever. ETEC is the most common cause of traveler’s diarrhea. * Enteroinvasive invade the mucosa (shigella. coli or cholera are secretory forms of diarrhea. metallic taste. These usually correlate with the underlying irritable bowel disease.56 - . * Extra-intestinal manifestations of IBD that do not follow the condition of the underlying bowel disease include ankylosing spondylitis (bamboo spine. reactive arthritis of small joints). The specific antibiotic for perianal fistula is metronidazole. probably in a traveler or people having anal intercourse. * Antibiotics often work in Crohn disease although it is not part of the official regimen and Crohn is not considered an infectious disease. the sulfasalazine link of sulfa to 5-ASA is cleaved at the distal ileum making the 5-ASA (mesalamine) available at the proximal colon. Entamoeba is a parasite typically in the ileum or colon. straight/flat back). young men typically present with jaundice and itching). Next step is steroids after mesalamine and antibiotics. Infliximab also approved in rheumatoid arthritis. gas. Symptoms are belching.5. Infectious Colitis * Infectious diarrhea occurs in enterotoxic and enteroinvasive. cobblestone appearance (more intense ulceration). proximal jejunum). hemoglobin is 6 grams. diarrhea. gastrin. Far more commonly in Crohn is a localized ileal resection. * Yersinia enterocolitica can mimic Crohn disease or appendicitis. nausea. With UC cancer you remove the entire colon. sacroiliitis. High grade dysplasia is confirmed by a second pathologist and treated like cancer. Saint Petersburg Russia. increases the risk of cancer. * Patient has blood diarrhea. If cancer. For entamoeba. * Enterotoxic (E. * If severe fistula disease not better with metronidazole or severe Crohn disease not getting better with medical treatment. * Crohn disease is treated similarly. Look for narrowing. Similar to Barrett esophagus. This is hemolytic uremic syndrome associated with E. * Secretagogue is something that causes secretion. skin involvement (erythema nodosum typically on lower extremity. looks ill. Secretory & Osmotic Diarrhea * Secretory diarrhea means there is some secretory drive for the intestine to put out lots of water. maybe hiking or drinking from a stream. ETEC E. * TMP-SMX works for most bacteria and quinolones work for nearly all causes of enterotoxic or enteroinvasive bacterial diarrhea. remove the entire colon. vomiting. you try to take out as little bowel as possible with Crohn disease. this is different than regular adenocarcinoma where you do a segmental resection. eye involvement (uveitis. maybe once every few weeks depending on patient. Salmonella can be enterotoxic in one form. coli O:157 (EHEC). next step is total proctocolectomy. Shigella dysentery has typical blood and pus in stool. * IBD. * All of these diagnoses are made by stool studies. * Giardia is a parasite that lives in upper intestine (duodenum. mouth ulcers (aphthous ulcers). typically traveling. remove entire colon. So if the patient has a lot of ileum involved and maybe jejunum.
appendectomy. which are yellow exudative plaques on the colon. go for sigmoidoscopy. * Stool Osmolar Gap is a calculation you will probably only see on the boards. This appearance does not look like anything else so you can tell the patient right there that they have pseudomembranous colitis. * Young female patient has supposed secretory diarrhea. If not very sick.000). There are also strains of vancomycin-resistant staphylococcus. gut tries to dilute non-absorbable lactose. probably secretory. * Pseudomembranous colitis associated with a very high white count (e. He is treated for 7 days with IV cefazolin with dramatic improvement in his symptoms. * Say you measure 2*(Na + K) as 274 and osmolarity is 350. Patient may have connection to the medical field (works in drug store. like cholecystectomy for vague symptoms. difficile. * Everyone with pseudomembranes on exam has C. difficile colitis includes clindamycin (most likely). * Most common osmotic agent is lactose. so this is an osmotic diarrhea. nurse). IV metronidazole gets into blood stream but not really to lumen of the gut. usually non-bloody. they don’t want to wait for a few days they want to know now so get your sigmoidoscope and get moving. difficile so hand-washing with soap and running water is required. 3 exploratory laparotomy operations. Stop antibiotics in these cases. WBC of 30-50. diff lives in the lumen of the gut so you want to clear it from the lumen of the gut. He has had diarrhea for the past 5 days. given oral. You may get called to the ICU for a very sick patient who has been on many antibiotics. Vancomycin is more expensive than metronidazole. colonic (left sided abdominal tenderness). * Direct way to make the diagnosis would be to put a sigmoidoscope in the patient and look for pseudomembranes. So not likely osmotic diarrhea. but not all patients with C.g. difficile. Add stool to plate. do a toxin assay. difficile does not grow in the gut but when you wipe out the normal flora with antibiotics the C. * Causes of C. If very sick patient. Medication causes include magnesiumcontaining drugs. Think factitious diarrhea. To get stool osmolality 2*(Na + K) so 274 here. or being exposed to diarrhea (nosocomial infection). difficile. There are also strains of VRE (vancomycin-resistant enterococcus) “superbugs” so metronidazole is first-line. diff can start to flourish. spectrum from well with mild diarrhea to very toxic-appearing with high fevers. * Most C. C. difficile make pseudomembranes. * If patient cannot tolerate metronidazole (e. * Treatment is metronidazole first-line. * In clinical practice. So besides the Na+ and K+ there is nothing else that has osmolar properties in the stool. etc. receiving antibiotics. salmonella. In a negative sigmoidoscopy. gold salts for rheumatoid disease. * C. terrible neuropathy) use vancomycin. * Now measure osmolality directly for the stool. difficile causes a secretory diarrhea. Enterocytes have villi and microvilli with lactase enzyme.g. colchicine. Patient may have multiple operations that they don’t have good reason for. stools bloody DO NOT DISTRIBUTE . close to 274. you can differentiate osmotic from secretory diarrhea from clinical presentation and initial laboratory testing.Study Notes – Internal Medicine James Lamberg 28Jul2010 calcitonin. paramedic. difficile patients do not have sky-high white counts. Say it is 275. Pseudomembranous Colitis * 59yo construction worker is admitted to the hospital for treatment of cellulitis that developed after dropping a steel beam on his leg. Normally C. Also cephalosporins or penicillins because we use those medications more than clindamycin.57 - . Exam shows vague mile left mid-abdominal pain. even if you’re a gastroenterologist. so the small intestine tries to dilute it by adding water into the lumen of the small bowel. Patient in the hospital is likely nosocomial or medications. if cytotoxic then we know it is coming from C. patient is taking laxatives. difficile are being in a hospitalized/nursing home setting. milk sugar. Ischemic Colitis * 72yo man complains of LLQ pain for the past few days. Next step is vancomycin. quinidine. antibiotics as a side-effect. PO (oral) is very effective. difficile colitis). so look at medication list for antibiotics. * Measure liquid stool sodium and potassium (if you can trick the lab tech into placing it into the machine where normally urine or serum goes) you’d get say Na+ 130 and K+ 7. and even that is not perfect because the spores are so sticky. can wait for toxin assay. You’ve done all the studies and hormone assays but found nothing. campylobacter in the hospital. but if it is present it points you to C. With lactase deficiency. * Ways to get C. * Antibiotic-associated colitis (non-pseudomembranous) is diarrhea associated with the change in flora that occurs with antibiotic use. * Osmotic diarrhea means there is an osmolar substance that is not absorbed in the small intestine. What is your next step in the evaluation of this patient? * Top of the differential list should be pseudomembranous colitis (C. so gap of 76mosm of something that does not belong there. He returns home and does fine until one week later when he has 6 watery green bowel movements a day and a low grade fever. Alcohol-based hand sanitizers do not remove C. * Patient do not develop shigella. Bacteria can ferment the lactose so patient can get a lot of gas and discomfort as well.
osteopenia/osteoporosis with no reason (e.Study Notes – Internal Medicine James Lamberg 28Jul2010 over last 48 hours. IX. * Mnemonic is FIC for folate. and has developed a temperature. * If IMA is lost. Where is the watershed area? At the splenic flexure. * Pathophysiology of celiac sprue is autoimmune disease with destruction of villi showing villous atrophy with DO NOT DISTRIBUTE . VII. or pulmonary embolism at one point. Less likely is ischemia.g. Patient might have both so the MCV might be normal but the width spread would be high (high RDW or RBC distribution width). where the hypogastric or internal iliac artery takes over. * Losing the SMA would infarct the entire small intestine. go straight to surgery. * Vitamin A deficiency will show disturbances in night vision and hyperkeratosis. get better with medical management. IMA has bloody diarrhea. diltiazem. Things absorbed only at the terminal ileum are B12 linked to intrinsic factor and bile salts. greasy or fatty looking stool. * Young patient with acute onset of diarrhea is most likely infectious. Malabsorption Syndromes * Lots of diseases can cause malabsorption. ileocolic. * Protein malabsorption signs are hypoalbuminemia and peripheral edema. negative stool studies. nonspecific pain. * Ischemic colitis should be at the top of your list in an elderly patient developing acute bloody diarrhea. increased food consumption. splenic. do an abdominal aortic angiogram. E. you see the localized or segmental colitis in the distal colon and sigmoid. * Most things absorbed past the ligament of Treitz. * SMA ischemia symptoms are centrally located abdominal pain that is out of proportion to physical exam. where the superior mesenteric artery (SMA) stops sending branches and IMA starts sending branches. but here we’re talking about malabsorption as the presenting symptom. What vessel is most likely involved? Inferior mesenteric artery (IMA) serving distal transverse colon to midrectum. digoxin use. metformin. patient may say they had to watch their diet as a kid and get food from special bakeries. * The small intestine does the absorption. patients generally get better. * Fat soluble vitamins are “in the attic”: A. What is the most likely diagnosis? Answer is ischemic colitis. * Celiac sprue is the most common cause of chronic malabsorption. factor VII has the shortest half-life * Three things if not absorbed in proximal ileum are not well compensated for are folate. high RDW). You would probably die from the gangrene and if you did survive you’d have to be on IV feedings forever. diarrhea. SMA feeds intestinal. Exam shows some tenderness. bad CHF with poor flow. elderly patient with atherosclerotic disease. History might be use of oral contraceptives. SMA has usually non-bloody diarrhea. The patient is writhing around as if they have a perforation. malodorous stool (due to fat). also in midrectum where IMA stops giving branches and hypogastric starts giving branches. We need grams of bile salts to absorb fats and 2/3 of those are reabsorbed in the ileum up to the liver (enterohepatic circulation).g. but now feels sick again (honeymoon period). glipizide. Vitamin E deficiency (rare) will show nystagmus and ataxia. irregular heart rhythm that puts patient at risk for thrombi (e. patient would have to be hypercoagulable since they likely do not have atherosclerotic disease. K.58 - . * Three major gut branches off the aorta are the celiac. and X. rectal exam reveals bloody stool. right colic. iron. atrial fibrillation). like celiac sprue. patient will have signs of FIC deficiency like megaloblastic anemia (folate deficiency) or hypochromic microcytic anemia (iron deficiency). calcium. Presents again as an adult. * Treatment is usually medical for IMA ischemia. acidosis (lactic acidosis from poor perfusion). Other thing on the list is infectious colitis. D. * If proximal small bowel is affected alone. or other hypercoagulable event with no risk factors. middle colic. so the malabsorbed material will be from the small intestine. Vitamin K deficiency measured by protime (PT) or INR. healthy young man. but abdominal exam is soft without guarding. * Malabsorption is an osmotic diarrhea. SMA. * Anisocytosis is the term used for mixed RBC widths (i. hypercoagulability (less likely). Patient may show signs of calcium deficiency like osteopenia or tetany (Chvostek or Trousseau sign). horrible central abdominal pain. aspirin. Vitamin D deficiency will show hypocalcemia. and calcium. If ischemia is present and severe. Celiac feeds gastric. leukocytosis. superior pancreaticoduodenal. Other major cause is tropical sprue. * Celiac sprue typically presents in childhood with malabsorption. History is significant for peripheral vascular disease and a myocardial infarction. needs angiogram then surgery. iron. * Ischemic bowel is a useless description since SMA and IMA ischemia are very different presentations. Patient is on isosorbide dinitrate. Vitamin K deficiency will show problems with clotting factors II. * Symptoms include weight loss. and IMA. * SMA ischemia risk factors include atherosclerotic heart disease.e. * If SMA ischemia is suspected. premenopausal woman). propranolol. hepatic. * Patient may have fever. This is the preperforation pre-gangrene stage. Less common (very rare) is Whipple disease.
this is pathognomonic for chronic pancreatitis. no villi. Diverticulosis & Diverticulitis * Diverticulosis can occur anywhere in the colon but usually it occurs in the sigmoid because that is the area of greatest pressure generation by the muscles of the large intestine (LaPlace law. no D-xylose in blood. X-ray plain film can show calcifications across the midline where the pancreas sits. and fat digesting enzymes like lipase. tetracycline. If you do a colonoscopy and see the diverticuli just leave them alone as long as patient is asymptomatic. also known as antitransglutaminase (tGT). LLQ post-prandial pain that resolves after bowel movements. pressure against pipe wall). * Treatment is broad antibiotics like metronidazole. Gliadin is a property of wheat. If normal absorption. This causes diverticulitis. * Most people over the age of 60 have diverticulosis but they are asymptomatic in general. But patient does not get better on gliadin-free diet and no anti-villi antibodies. * Most common disease causing insufficient pancreatic enzymes is chronic alcoholic pancreatitis. There will be inflammatory cell infiltration such as lymphocytes. you need the clinical features too. * Diverticuli can rupture or perforate. and no bleeding. * A viral gastroenteritis can wipe out the villi for a few days but they come back in a week or so. older test and less specific. proteolytic enzymes like trypsin. joint involvement. If bad perforation. patient gets fecal peritonitis and will be very sick. * Whipple disease diagnosis confirmed on small bowel biopsy showing PAS-positive macrophages. there will be D-xylose above a certain level in bloodstream. tetracycline. If no absorption. Say you see 50g/day then the patient is malabsorbing fat. skin involvement (hyperpigmentation). no D-xylose in urine if malabsorption). * Definitive diagnosis is based on small bowel biopsy. Treat with high fiber diets to make stools bulkier giving some symptomatic relief. specific). India. where it gets weighted for large volume then measured for fat. * D-xylose depends on nothing except an intact small bowel.59 - . LLQ findings on an exam even looking like a left-sided appendicitis (appendix is just a diverticulum on the right side). * Testing for malabsorption in general includes the 72h fecal fat collection. inflammation. * Celiac sprue antibodies are against villi. plasma cells. and rye. Also anti-gliadin antibodies seen in sprue. After removing gliadin from diet the villi grow back. So the diagnosis of sprue is not made from villous atrophy alone. tenderness. Could also do a 5h urine collection (D-xylose in urine if normal. LLQ pain of relatively acute onset. Some patients can’t tolerate oats either. * Test for small bowel absorption is the D-xylose test. elastase. * Treatment is follow non-gliadin diet. cardiac involvement. Small bowel absorption in chronic pancreatitis would be normal. spilling fecal contents out. 50g of D-xylose powder is added to water and patient drinks it. fluoroquinolone. * Treatment for Whipple disease is broad-spectrum antibiotics like metronidazole. More likely to get this done at home. * Whipple disease presents as malabsorption symptoms plus other organ involvement. It looks like celiac sprue if you were to do a small bowel biopsy. The patient would put lots of fat into the 72h stool collection. the diverticuli don’t bleed to give iron deficiency anemia or guaiac positive stool. barley. So these patients will have B12 deficiency showing megaloblastic anemia. chemotropism. Patient presents with brisk arterial bleed. * Diverticular bleeding can occur in the dome of the diverticuli. but it is rare that you get one of these completed in the hospital because the collection can will stink up the entire room by the third day. look for anti-endomysial (most sensitive. leukocytosis. lymphadenopathy. * Major enzyme classes all come from pancreas: amylase to digest carbohydrates. * Diverticulitis is usually in an older patient. * Tropical sprue affects distal small bowel. blood measured 2h later. Asia) who comes back and now has malabsorptive symptoms. fluoroquinolones. * Tropical sprue affect patients in the tropics (Caribbean. D-xylose is a sweet tasting sugar that does not appear in the regular diet. Example would be CNS involvement (dementia). Celiac sprue patients also get megaloblastic anemia but that is due to folate. fever. This is exocrine insufficiency of the pancreas. Tropheryma whipplei bacteria can be seen on electron microscopy. you should have less than 7g/day of fat in the stool. where B12 is absorbed. Tell patient to eat a diet with a lot of fat (100g/day) and collect the stinking steatorrhea stool and go to the lab. If the rupture is well contained you can see bowel wall thickening on CT scan. This prevent the malabsorption and the long-term complication including intestinal lymphoma and intestinal adenocarcinoma.Study Notes – Internal Medicine James Lamberg 28Jul2010 blunting or complete loss of villi showing crypt hyperplasia. hematochezia). Even on a high fat diet. There is no need for active transport or breakdown by digestive enzymes. If not well contained you can see abscess in the wall of the colon (intramural abscess) or more severe pericolonic abscess. they present with sudden painless bright red blood per rectum (BRBPR. * Diverticular spasm due to contraction against hard stools can cause pain. localized rebound. DO NOT DISTRIBUTE .
* Peutz-Jegher is non-adenomatous polyps. they are hamartomas. Breast cancer is most common in non-smoking women and second most common in all women. change in bowel habits (constipation). bone tumors. * Most common cause of cancer in women is lung cancer. third is colorectal cancer. ovarian cancer). thin caliber stools (“pencil thin”). Do most of those patients actually have colon cancer? No. * If family history is strong with adenocarcinomas. With mammography we hope to detect early cancer.Study Notes – Internal Medicine James Lamberg 28Jul2010 * Diverticulitis is a localized perforation with abscess and no bleeding. adenomatous polyps. Fluoroquinolones used as well. * Diverticulitis diagnostic test is CT scan. * Diagnostic test for Hirschsprung is barium enema showing dilatation of colon above tight contracted sphincter. hereditary polyposis syndromes (familial polyposis coli. * The only preventable cancer of those top three is colorectal cancer. * Older patient with blood in the stool. Prostate cancer is next. we find the cancer not the precancer. we treat with IV antibiotics effective against anaerobes and gram-negatives like ampicillin. * Everyone should have an annual digital rectal examination beginning at age 40. Constipation in children is most commonly caused by regular constipation. family history of colorectal cancer. In lung cancer. * Any older person with iron deficiency has colon cancer until proven otherwise. Chagas can also cause cardiomyopathy and myocarditis. These patients get early colorectal cancer screening. * Screening tests can change over time. BPH is not a pre-cursor. but it is still cancer. * Regular constipation can be treated with increased fiber and laxatives. it depends on the patient’s normal daily bowel movements. everyone should get a barium enema and flexible sigmoidoscopy at age 50. abdominal pain. Most recommendations say colonoscopy at age 50 for everyone because it is more sensitive and allows you to manage the polyps that you find. * Risk factors for sporadic colorectal cancer include Western diet (low fiber. extensive Crohn disease. Occult blood with guaiac testing should occur annual beginning at age 50. desmoid tumors. * Juvenile polyposis syndromes are also hamartomas. DO NOT DISTRIBUTE . Better measurement would be too few bowel movements and bowel movements that are too hard. autosomal dominant. tumors of papilla of Vader. not adenomas. The baby is squeezing to empty their bowel and over time the more proximal bowel gets dilated. think about hereditary non-polyposis cancer syndromes. autosomal dominant). * If diffuse peritonitis. Early screening if family history. non-polyposis familial cancer syndromes (Lynch syndrome. Patients develop colorectal neoplasms at a younger age and with a higher likelihood. 90% or more of colorectal cancer is sporadic where the only history is polyps and/or first degree relative with polyps or colorectal cancer. We could eliminate colorectal cancer (except familial forms) if we removed every adenomatous polyp in this country. * Hirschsprung disease is a congenital loss of the myenteric plexus and the internal anal sphincter fails to relax. high red meat). metronidazole. With severe constipation though. osteomas of the skull. ulcerative colitis. no leukocytosis. worry about Hirschsprung. PSA or prostate biopsies are not pre-cursor lesions. iron deficiency anemia (might be first symptom). Constipation is a broad workup however. Specific genetic defect. At the least. * Test of choice if you suspect colorectal cancer is colonoscopy. * Hirschsprung disease is rare in children and even more rare in adults. Even now your screening could depend on what organization’s recommendations you follow. no fever. * Most common cause of cancer is men is lung cancer. distention (if well advanced). You can remove polyps and biopsy any mass. * Older patient with acute change in bowel habits (constipation) think colon cancer until proven otherwise. * The premalignant condition for colon cancer is the adenomatous polyp. Diagnosis is confirmed with full-thickness biopsy of rectum showing loss of myenteric plexus. Here we are discussing diseases that present with constipation as the primary symptom. Diverticulosis can be sigmoidoscopy.60 - . and third-generation cephalosporin. Do not confuse this with diverticular bleeding presenting with hematochezia. start IV antibiotics and go to surgery to clean up mess and resect area that is perforated. breast cancer. * Gardner syndrome is large bowel cancer with non-colonic involvement. pancreatic cancer. Colorectal cancer is second most common in non-smoking women and third most common in all women. generally resected. Gentamycin not used much. In colorectal cancer we are finding a truly premalignant condition that we can remove and eliminate the cancer risk. hyperpigmentation around lip corners. Treatment is surgery. Constipation & Colorectal Cancer * Constipation is defined as less than three bowel movements in a week. * Chagas disease (Trypanosoma cruzi) can cause megacolon and achalasia pattern due to loss of myenteric plexus from acetylcholine fibers. but it might be difficult to see when blood is coming at you. * If patient not too sick. soft tissue tumors. * Do not do endoscopy or barium/air enema with suspected diverticulitis because you can worsen the perforation. Rule-out hemorrhoids then maybe CT scan if cannot do sigmoidoscopy. but you cannot miss this diagnosis.
They will say if it is tubular histology or villous histology. Gastrointestinal Bleeding * Upper GI bleeding means the bleeding is originating from proximal to the ligament of Treitz. Colonoscopy involves IV sedation so there is risk there too. such as alcoholic liver disease or hepatitis C induced cirrhosis. which is the junction of the duodenum and jejunum. hemorrhoids too. submucosa. the muscularis mucosa. Patients can tolerate these medications so useful for outpatient chemotherapy from 6 months to a year. * Duke C is the staging that has increased survival with chemotherapy. anastomosis of colon ends together. * Radiation is useful for advanced rectal cancers. and even hematochezia since blood is a GI irritant and would have rapid GI transit. hematemesis. * Polyp seen on colonoscopy can be sessile (broad base on wall) or pedunculated (on a stalk). * If polyp is hyperplastic. * Anal cancer is squamous cell. Beyond the duodenal bulb acid is neutralized so you do not get ulcers there. Tubular is a histologic description. either pre-op or post-op to improve long term survival. patient has to come back to make sure no new polyps have grown back. B1 means not full thickness. goes locally to lymph nodes then liver (not lungs or bones without going through liver first as a rule). C1 means not full thickness and with lymph nodes. maybe chemotherapy depending on the stage of rectal cancer. black tarry foulsmelling stool). * The better we get with colon cancer screening and polyp removal. Squamous mucosa does respond to chemotherapy and radiation. pathologist will give you additional information. HPV warts (condyloma accuminata) are precursors to anal cancer. Duke B is controversial. * Duke A cancer is limited to the mucosa. do not call it tubular because it looks like it has a tube. * If biopsy of a polyp (polyp not removed) and it is adenoma then you need to go back and complete the polypectomy. B2 maybe. Rectal cancer on the other hand needs surgery and radiation. the less likely Americans are to die from colon cancer. * Presentation can be coffee ground emesis (blood). send blood for type and cross. C2 means full thickness with lymph nodes. patient needs to go to surgery and have cancer removed with clean margins on each side and management of blood vessels. Then you would have to do a complete colonoscopy to clear colon. Villous histology has a higher potential to become malignant. you have to remove the cancer first before chemo. * Duke D cancer is distant metastasis. B2 means full thickness but not through. * Duke B cancer goes into layers of the bowel wall but not through it. * Virtual colonoscopy is a CT scan of the colon and is not standard of practice currently. or duodenal bulb. * When do we give chemo? Duke A patient is cured so not needed. Most upper GI bleeds are near the esophagus. * Other causes of dark or black stool are patients taking iron supplements and patients taking oral bismuth. Mallory-Weiss tears. Early anal cancers can be cured without surgery using chemotherapy and radiation instead. then think about whether the patient needs chemotherapy or not. Duke D patient is too late. * Cause of upper GI bleeds include esophageal varicose veins. * Chemotherapy drugs for colorectal neoplasm are 5-fluorouracil (5-FU) and leucovorin (folinic acid) or levamisole. get blood bank ready if needed. * Any cause of upper GI bleed patient will become tachycardic and have orthostatic hypotension with volume loss then hypotensive and shock-like symptoms with further blood loss. * Duke C cancer does not go through full thickness but has lymph nodes. HPV is the precursor to cervical cancer in women. Interval is controversial. * First step in management of active GI bleeding is start large bore IV and give volume. stomach. The veins are collateral circulation that become engorged. Leucovorin is used as adjuvant therapy working synergistically with 5-FU. * Malignancy found on colonoscopy. Upper GI barium series has no role in the management of active upper GI DO NOT DISTRIBUTE .Study Notes – Internal Medicine James Lamberg 28Jul2010 * Around 30% of Americans have adenomatous polyps after the age of 50. past mucosal layer. B1 no chemo.61 - . * Negative colonoscopy at age 50. * If polyp is adenoma. patient can wait 10 years until next colonoscopy. Chemo should be given for Duke C as the cancer is localized but not systemic. A couple decades from now colon cancer may be deeper down the list instead of the third most common cancer in men and women. Example would be a general surgeon or non-gastroenterologist doing a sigmoidoscopy and doing a biopsy of a polyp instead of polypectomy. patient cured almost for sure with surgical resection. * Sigmoidoscopy with barium enema is less expensive and less likely to have a complication such as a perforation. * If adenoma polyp is found. * Test of choice is upper GI endoscopy. * Varicose veins is due to portal hypertension from liver disease. Layers are mucosa. say 3-5 years if small polyp. it is not premalignant. particularly seen in homosexual men with HIV. ulcer disease. * Chemotherapy is never curative for colon cancer. melena (acid degrading blood.
give fluid. typicaly AVM.Study Notes – Internal Medicine James Lamberg 28Jul2010 bleeding. You should not see a blush or collection on the right side. or during the prep the bleeding could have stopped. If the patient continues to bleed. just formed brown stool. can be done laparoscopically. type and cross blood. given as IV bolus then hourly infusion typically for three days if the patient has esophageal variceal bleeding. Octreotide is 8 peptides. Say the patient his diverticuli along the whole colon and you see lots of blood on colonoscopy. * A clue that rectal blood is from an upper GI bleed is an increased BUN/Cr ratio. next step is stabilization. Treatment is resection. Blood is not absorbed in the colon so BUN/Cr would not increased with a straight colonic bleed. in between) is likely colonic bleeding. It is done if the nuclear scan cannot be done or the nuclear scan is not diagnostic. * If major bleeding. endoscopist can inject a sclerosing agent or place rubber bands over veins (banding). Exam shows tenderness in mid-epigastric region. Exception is variceal bleeding. BUN/Cr around 40:1 because small intestine absorbs some of the blood and breaks it down to urea. * You can do a sigmoidoscopy first in a patient that is actively bleeding because you do not necessarily need to prep the patient (bowel prep). * Say you do flexible sigmoidoscopy and it is non-diagnostic. AVMs more commonly seen in patients with aortic stenosis (controversial idea). AVMs usually found in ascending right side of colon. Start large bore IV(s). * Most diverticular bleeds stop spontaneously and do not require surgery. Sigmoidoscopy can be done immediately. * If the bleeding scan is non-diagnostic and the patient continues to bleed from diverticular disease. IV PPIs might help. Endoscopy allows you to make the immediate diagnosis and even treat the source. * Angiography is rarely used. Many people have diverticuli that do not bleed. called Meckel scan. usually epigastric with/without radiation to back. injected back into the patient. physician can inject the blood vessel locally with the angiogram catheter or maybe put a coil in to stop the bleeding. Also nuclear scan is less invasive and can be repeated over several hours. A local external exam or short-scope anoscopy can show hemorrhoids or fissures that are bleeding. * A red blood cell scan in the abdomen should show you the vasculature normally. painless bleeding. we generally send the patient to surgery. angiodysplasia was previous name). Next step if the patient is actively bleeding is a bleeding scan where nuclear label is mixed with the patient’s red blood cells. so you see the bleeding diverticuli then go higher and see no blood. associated with nausea and vomiting. Alcohol is a direct toxin to the pancreas DO NOT DISTRIBUTE . which would imply right colon. You would see gastric cells light-up in the small bowel. then looking for the bleeding source. An angiogram requires active bleeding to be positive. Gastric mucosa arrives in the diverticulum and acid production can cause ulceration of the diverticulum causing bleeding. you should suspect Meckel diverticulum. * Hematochezia or maroon stool (not BRBPR. which is why the nuclear scan is done first. * Management of choice is endoscopic hemostasis. the surgeon is stuck and has to do a sub-total colectomy taking out the whole colon down to the rectum. Hopefully the bleeding scan pinpoints the area for localized resection. * Medical therapy is not as useful for controlling GI bleeding. * Diverticulosis usually found in sigmoid. Bleeding events may be episodic. so if you see them do not assume that was the cause. In elderly. * Exception is children or young adults with negative colon testing and painless blood emanating through ileocecal valve. then the bleeding scan can help localize the problem area. sometimes diffuse tenderness. if the cells are leaking out somewhere they will accumulate in that area. Octreotide is a synthetic analog of somatostatin and reduces portal pressures. * Most common cause of mild (small amount) painless rectal bleeding is hemorrhoids or fissures. * Lower GI bleeding is defined as distal to the ligament of Treitz. Another use of angiography would be an active bleed where you are worried about the patient sitting in nuclear medicine for a while as they might bleed too much. That tells you that the blood is occurring from a distal area and since there is lots of blood in the region of the diverticuli you assume this is a diverticular bleed. You do colonoscopy and it is non-diagnostic. * Medical management for esophageal varices specifically is octreotide. It requires more active bleeding than a nuclear scan.62 - . * The colonoscopy can show the location of the bleed. * Nearly all cases of acute pancreatitis are caused by alcohol or gallstones. the aorta and internal iliacs. they require a resection. * Management is to prep the patient for a colonoscopy (bowel prep) then do a colonoscopy as bleeding can occur all the way to the right colon. * If esophageal varices. so BUN raises out of proportion to creatinine. * During angiography. If the patient stops bleeding from diverticular disease and then restarts. next most common is diverticulosis then arteriovenous malformations (AVMs. no melena. Pancreatitis * Acute pancreatitis presents as abdominal pain. You can see anorectal bleeding or on occasion see diverticular bleeding. * Diagnosis of Meckel diverticulum done with a bleeding scan that labels gastric mucosa. but very few things bleed in the small intestine. but might not be diagnostic.
bilirubin producing a yellow color. They can present with endocrine insufficiency as diabetes with insulin dependence from beta cell destruction. * Treatment for cholangitis should also include antibiotics. biliverdin producing a green color. Bilirubin bound to albumin travels via portal system to liver hepatocytes where it is conjugated to glucuronic acid giving bilirubin glucuronide. AST. sequestration of fluid > 6L. Crigler-Najjar. Bilirubin is also metabolized here. * RBCs last about 120 days and get trapped in spleen in the reticuloendothelial system as they break down. you may need to do follow-up CT scans and drain any new cysts/abscesses. Disruption of the duct with severe pancreatitis will release fluid that forms into a cyst called a pseudocyst (pseudo because not lined with true epithelial cells). fever. Cholangitis is classically with Charcot triad of RUQ pain. Severe pancreatitis is likely if score 3+. Heme part of RBCs is broken down to biliverdin then to bilirubin. * Initial labs should include amylase and lipase. do a CT scan to rule out pancreatic abscess. * If patient is not getting better after a few days of NPO and IV fluids for pancreatitis. age. glucose. * Gilbert (pronounced jheel-BAYR). LDH. * Gallstone pancreatitis is usually associated with a history of biliary colic (crampy RUQ pain after meals). * Say total bilirubin is 5. then you know this is not a liver problem (spleen problem. patient can get an operation called a Puestow procedure. hemolysis). correction of hypochloremic hypokalemic metabolic acidosis. If the pain is very severe. NPO because food stimulates the pancreas.63 - . * Puestow procedure (longitudinal pancreaticojejunostomy) can be useful to prevent narcotic addition or to help a patient who is already addicted to prescription narcotics. * Total bilirubin is direct + indirect bilirubin. * Inflamed swollen boggy pancreas is called a phlegmon (spreading diffuse inflammatory process with formation of suppurative/purulent exudate or pus). meets with splenic vein into the portal vein and through liver.8. * Gallstone pancreatitis never leads to chronic pancreatitis because patient either gets better or goes for stone extraction with ERCP. Chronic pancreatitis is usually associated with alcohol use. which is problematic because in general they are alcohol addicts and you run the risk of making them narcotic addicts from iatrogenic prescribing. which was originally developed just for alcoholic pancreatitis. Direct is conjugated bilirubin. Then you know most of the bilirubin is unconjugated. * The SMA feeds the small intestine and the SMV. * Mnemonic (48 hours): C HOBBS. WBC count. Indirect is unconjugated bilirubin. Say total bilirubin is 10 and indirect is 9. All the proteolytic enzymes cannot leave the pancreas so you get autodigestion of the pancreas by the enzymes. calcium. and jaundice. That bilirubin is the one that ends up in your bloodstream making you yellow or into kidneys making urine tea or cola colored.0 and indirect is 3. Liver Disease * Liver is an important synthetic site for many compounds such as albumin and coagulation factors. * Treatment of gallstone pancreatitis that does not resolve on its own is endoscopic retrograde cholangiopancreatography (ERCP) with stone removal. * Blood test abnormalities are described in Ranson prognostic criteria. A stone would need to block either the common bile duct and/or the pancreatic duct (choledocholithiasis). Initial testing can include CT scan. exocrine pancreatic insufficiency. now pancreatic enzymes drain right into the jejunum preventing irritation of the pancreas from trapped enzymes. * Mnemonic (admission): GA LAW. lipase is more specific. pain. Calcium becomes deposited through duct system of the pancreas and can be seen on plain film indicating chronic calcifying pancreatitis. Other important symptom of chronic pancreatitis is chronic abdominal pain. For ICU patients. * Treatment is to put the pancreas at rest. Bilirubin may climb to 5 or 6 here. base deficit. Mortality 100% if score 7 or 8. Albumin bound bilirubin coming out of spleen is not water soluble and is not urinated. It is also an important detoxification organ and nutrition absorption organ. fistulization into the lung causing pleural effusion (send fluid for amylase). IV hydration. * Common bile duct obstruction with cholangitis should be treated via ERCP stone extraction. and Dubin-Johnson syndrome are problems with indirect DO NOT DISTRIBUTE . hematocrit. thus high unconjugated bilirubin will not darken the urine. it is due to chronic pancreatitis. Bile and even pus may pour out and patient gets better. * Chronic pancreatitis can present with exocrine insufficiency as maldigestion and we treat them with pancreatic enzyme replacement. NG tube if need to decompress the stomach (if vomiting). and localized pancreatic abscess occurring in a few days. they need surgical debridement of the abscess or even radiology-guided needle aspiration. O2. with hemoglobin itself producing a red-blue color. and hemosiderin producing a golden-brown color. If pancreatic abscess. BUN. after taking in intestinal nutrients.Study Notes – Internal Medicine James Lamberg 28Jul2010 causing inflammation. Procedure filets open the pancreas then sew a loop of jejunum into the bottom of the pancreas. so insulin dependent diabetes but not Type I. Pseudocyst can cause obstruction. * The colors of a bruise are caused by the phagocytosis and sequential degradation of hemoglobin to biliverdin to bilirubin to hemosiderin.
Do not confuse PSC with PBC. Crigler-Najjar presents at birth and requires major medical and surgical therapy (phototherapy 12h/day. * Hepatitis A vaccine exists. With a mechanical blockage of the bile duct we have conjugated bilirubin backing up into the bloodstream making you jaundice. electrolytes. Patient presents with pruritus as the earliest symptom. * Alpha1-antitrypsin deficiency leads to unopposed action of trypsin which is a proteolytic enzyme. Tell patient about the syndrome to help prevent medical testing in the future (ultrasounds. The bile salts in the bile give you the pruritus. * Younger man presenting with pruritus. no signs of hemolysis. DO NOT DISTRIBUTE . Liver transplantation is curative. Incubation period is a couple of weeks. Organs affected are liver and lung. scleral icterus) at times of stress. Gene for alpha1-antitrypsin is located in liver so new liver corrects the problem. can be transmitted via seafood. Viral Hepatitis * Hepatitis A can be asymptomatic and IgM (active infection) positive. As this disease progresses the patient will need liver transplantation. Antibody that is positive but not too useful in diagnosis is ANCA. low grade fevers. Family history of liver disease. Example scenario would be a nursing home or kindergarten outbreak where kids and teachers get jaundice. Organs are liver. anorexia. Organs include eye (Kayser-Fleischer ring). bilirubin. biopsies). Diagnosis is via liver biopsy. * Wilson disease is a problem with excess copper deposition in the liver due to poor excretion from GI tract in bile. Typical symptoms of hepatitis are jaundice. This is almost always seen in middle-aged women (40s-60s). low levels of ceruloplasmin (copper carrying protein). Suspect in patients who have emphysema and are non-smokers or if patient has relatives with precocious emphysema. Dubin-Johnson prognosis is much better with most patients living normal lives. such as intrahepatic stricturing or stone. get before you travel to endemic areas or get because universally recommended. Diagnosis confirmed by liver biopsy staining for copper (Timm silver stain). high copper in 24h urine. malaise. * Autoimmune disease against the microscopic bile ductules is primary biliary cirrhosis (PBC). seeing damage to microscopic bile ducts. Chief problem with Gilbert syndrome is you see the bilirubin (2-4. * Hemochromatosis is hyper-absorption of iron in the intestine and deposits of iron in various organs. ALP is the first blood test to become elevated. transfusions). dementia). fevers. Eventually patient will get cirrhosis from this. Patient is asymptomatic but may get mild jaundice (e. Past exposure can be seen with IgG antibody. * Hemochromatosis. All can progress to cirrhosis and end stage liver disease. * Treatment of alpha1-antitrypsin is limited. Then the patient becomes jaundiced (elevated conjugated bilirubin). Hepatitis A is fecal oral. Bile contains water. Most cases are mild. Past major cases involved strawberries and green onions. Screening test is high serum iron to total iron binding capacity ratio (Fe/TIBC) up to 90% even and a high serum ferritin (lots of blood iron). Bile salts are also conjugated and hydroxylated. If patient has progressed to cirrhosis and portal hypertension. which is copper chelation from bloodstream. there will be a high indirect bilirubin. * Blockage of the common bile duct. post-mortem liver may look black or dark-pink. liver disease. fatigue. They all have another organ involvement to suggest them. PSC is associated with ulcerative colitis. Classic is stricturing and narrowing of the biliary tree. RUQ tenderness. The only one you will probably see in clinical practice is Gilbert syndrome. would lead to jaundice and pruritus. so biopsy not need but a picture of the ducts is needed. There is likely a family history of liver disease. Labs show high serum copper. increased ALP. Test of choice is ERCP with dye injection to visualize biliary tree.g. This is sclerosing of the larger macroscopic bile ducts. Ultimate diagnosis rests in liver biopsy.64 - . Other drugs include zinc and triene. Bile salts derive from cholesterol synthesis and are needed for fat digestion. Gilbert syndrome is a problem with the uptake and conjugation due to deficiency of glucuronyltransferase. separate process from bilirubin. Diagnosis is via liver biopsy and stains for iron on that biopsy (Prussian blue). * Treatment of hemochromatosis is weekly or monthly phlebotomy to make the patient borderline iron deficient thus bone marrow is hungry for iron and pulls it out of the organs. Autoimmune marker is anti-mitochondrial antibody is suggestive. they will need liver transplantation which is curative. Reticulocyte count is normal. showing beads on a string pattern. liver transplant. Wilson disease. increased bilirubin. Management at that point is liver transplantation. pancreas. * Hepatitis A does not become chronic so patients cannot get cirrhotic or get a hepatoma. * PBC treatments do not work very well and patients will get cirrhosis at some point. Blood test is alpha1-antitrypsin level. Trypsin originates in the liver and is inactivated by alph1-antitrypsin. Disease is primary sclerosing cholangitis (PSC).Study Notes – Internal Medicine James Lamberg 28Jul2010 bilirubin. almost all indirect) and worry about liver problems. * Treatment of Wilson disease is penicillamine. CNS (choreoathetosis. skin (“bronze diabetes”). and alpha1-antitrypsin deficiency are hereditary liver disease. and bile salts. Test to do is hepatitis A IgM. but know penicillamine. liver transplantation if needed and for cure. * Crigler-Najjar and Dubin-Johnson syndrome are very rare and are problems secreting bilirubin from the hepatocyte. heart (cardiomyopathy).
65 - . do an MRI of the pituitary to look for the lesion. True hepatitis infection in the past would be HBsAb and HBcAb. TRH activates TSH release and that activates T3/T4 release from thyroid. IV drug abusers. * 32yo woman comes to your office because she has noticed a milk-like discharge from her breast for the past four weeks. They secrete autonomous prolactin. -------------------------------------------------------------------------------------------------------------------------------------------Kaplan Videos (2001) – Endocrinology with Dr. and pressure phenomenon. Treatment used for moderate hepatitis C prior to cirrhosis progression. and end organs. Examination reveals galactorrhea but is otherwise normal (no visual field cuts or amenorrhea). Usually adenohypophysis secretes hormones that affect organs in the periphery. secreting hormones (ACTH. Prolactin is under continuous inhibition from dopamine. pre-1989 via transfusion or needlestick injury or dialysis worker or IV drug abuser. eventually cirrhosis and hepatoma (hepatocellular carcinoma). * There is a hepatitis B vaccine. Interferon can be used as well. Also others like adefovir.hemianopsia. It is seen in epidemics. TRH is not tested for because it is expensive and has to be sent out. * Medical treatment for hepatitis C is pretty good. do liver biopsy to assess activity. tenofovir. No need to treat everyone. Stages of control are hypothalamus. * Treatment of prolactinomas is bromocriptine. Thus there is minimal pressure phenomenon. * Pituitary is divided into posterior and adenohypophysis. Suspect hepatitis D in severe cases of hepatitis B. If after six month of HBsAg positive without HBsAb. TRH at high doses seems to be an activator of prolactin. * In men. Transaminases increased are SGOT (AST) and SGPT (ALT) from 50 up to 200 max. If progressed to cirrhosis then it is too late to treat. you are labeled as chronic hepatitis B. jaundice. So pituitary disease commonly affects visual field. MD -------------------------------------------------------------------------------------------------------------------------------------------Pituitary Disease: Hyperpituitarism * Pituitary gland is on the sella turcica surrounded by the sphenoid bone and around that area is the optic chiasm. In a normal individual hormone. * Hepatitis E has a high mortality in pregnant women. hepatitis B surface antibody (HBsAb) and hepatitis B core antibody (HBcAb). * Hepatitis B transmitted via blood or sexual contact. TSH is up and TRH is up. * Medical treatment for hepatitis B includes antiviral drugs lamivudine. think prolactinoma because these are the most common active pituitary tumors. which has low T3 and low T4. Hopefully you become immune if you body creates the appropriate antibodies. etc) and is affected directly by other hormones in the hypothalamus. the prolactinoma is usually a microadenoma. * Hepatitis D is a co-infection with hepatitis B. TSH. The low T3 and T4 go back as positive feedback to pituitary to increase TSH and also goes into hypothalamus to increase thyroid releasing hormone (TRH). Test is PCR for hepatitis C where we can measure quantitatively how much hepatitis C there is. Posterior pituitary secrets oxytocin and ADH. Decreasing production of prolactin from a prolactinoma would shrink the size of the tumor. When dopamine is inhibited or if autonomous adenoma will you get prolactinemia. It is fecal-oral and not common in the United States. They usually presents with amenorrhea and galactorrhea +/. do not jump to adenoma as the cause. * Hepatitis C presents with chronic fatigue and chronic transaminase elevation. or chronic hepatitis B that has become newly activated. headaches. Hepatitis B can become chronic and thus develop cirrhosis and hepatoma (hepatocellular carcinoma). They usually present with visual field cuts. which are produced by the hypothalamus and stored in the pituitary. Look for other causes like dopamine inhibitors like haloperidol (depletes dopamine) and primary hypothyroidism. RUQ pain. With primary hypothyroidism. specifically bitemporal hemianopsia. prostitutes. and entecavir. pituitary. give alpha-interferon subcutaneously and ribavirin. * Hepatitis C transmitted via blood usually. typically seen in patients with a high titer of hepatitis B like patients who continually use IV drugs. * With galactorrhea presentation. Check for TSH. She is on no dopamine depleting medications and has a normal TSH and T4. * If prolactin level is elevated. it usually does not present acutely. Getting the vaccine only would be HBsAb without HBcAb (surface without core). fevers. If minimal activity then might not need treatment. fatigue.Study Notes – Internal Medicine James Lamberg 28Jul2010 * Hepatitis B patients are generally symptomatic. Every case of hepatitis C becomes chronic. * In women. etc. Active infection serology is hepatitis B surface antigen positive (HBsAg). There is no vaccine for hepatitis C. * 32yo woman comes in with galactorrhea. DO NOT DISTRIBUTE . What is the next test to order? Answer is prolactin level. Charles Faselis. There is not much we can do about hepatitis D. a major risk for health care workers. alpha-interferon with ribavirin. which is a dopamine activator and thus a prolactin inhibitor. telbivudine. the prolactinoma is usually a macroadenoma. They rarely present with gynecomastia or galactorrhea. * With galactorrhea. Anyone exposed to blood or sexual contact should be vaccinated so health care workers.
cancers. prolactinomas occur in older women. you are not worried about pregnancy so you can watch the patient and not treat if there is no pressure phenomenon. but the ADH cannot work because the DO NOT DISTRIBUTE . These patients had no endocrine issue but got a CT or MRI for another procedure and were found to have an empty sella. * In rare scenarios. and organs grow such as the heart which leads to congestive heart failure and is the most common cause of death. called central diabetes insipidus (CDI). Screening test for acromegaly is to give the patient glucose then measure growth hormone after an hour. The first sign of Sheehan syndrome is the inability to lactate. any space occupying lesion can cause hypopituitarism. shoe size. * Glucose causes the release of insulin and counter-regulatory hormones like growth hormone. which has an effect on tissue and bone causing it to grow. ILGF are somatomedins. * Treatment of pituitary apoplexy is medical stabilization. and trauma to the head. high cortisol. and cortisol. which shrinks the size of the tumor in acromegaly for unknown reasons. So the pituitary is pushed off to the side and squished between the meninges. growth hormone is elevated. vomiting. granulomas in the brain. glucagon. If it looks like Sheehan syndrome. This can occur even 5 years after pregnancy. larger feet. normal response is decrease in growth hormone. In adults. History is patient with pituitary adenoma comes in with stupor. The most common in children is a craniopharyngioma. * Patients with empty sella syndrome usually have normal endocrine function. Pituitary Disease: Posterior Pituitary * Diabetes insipidus (DI) occurs when patients are missing the major water-retaining hormone in their body. and headaches. In empty sella syndrome. tumors in the brain. You do not just measure GH because it changes throughout the day so you have to provoke it. * We could also measure ILGF levels. and growth hormone. CDI can occur with any space occupying lesion or anything affecting the central nervous system. thus cannot be easily visualized on CT or MRI. do the insulin tolerance test to make sure it is not hypopituitarism. which is a bit more important. it would be stroke syndromes. Growth hormone mainly works through the liver by secreting insulin-like growth factor (ILGF. If GH is not high an hour after 5U insulin given. * 80% of acromegaly patients have elevated glucose and about 30% of them have diabetes mellitus. Next treatment option is bromocriptine. * In children. Give patient 5U of insulin to cause hypoglycemia. * Pituitary apoplexy is a medical emergency. else you lose free water. In this case. Acromegaly is due to hypersecretion of growth hormone. * Nephrogenic diabetes insipidus (NDI) occurs when ADH is in high levels. You can also check the levels of FSH and LH in the blood. * Acromegaly with pituitary adenoma is caused by a macroadenoma 75% of the time. The first hormones to be lost are the ones you need the least. Surgery and radiotherapy are also options. tongue grows.Study Notes – Internal Medicine James Lamberg 28Jul2010 * Treatment of prolactinomas that are macroadenomas (usually men) may need surgery or radiotherapy. which would always be elevated in acromegaly patients. Somatostatin is a statin of somatic activity. You cannot have empty sella syndrome with normal endocrine function. Counter-regulatory hormones keeps glucose levels high in the blood. namely stroke syndromes. * Sheehan syndrome usually occurs after a prolonged and labored pregnancy. Insulin puts glucose into cells and lowers blood glucose. * Acromegaly symptoms are enlarged head. Lastly you lose the most important. Appropriate response is no insulin release and elevated counter-regulatory hormones. or mediators of somatic activity. * Before considering a MRI of the pituitary (80-90% of cases) in acromegaly. the patient is missing the diaphragmatic surfaces holding the pituitary in. antidiuretic hormone (ADH). If glucose is high. It may occur because the patient is missing ADH. Then TSH is lost. jaw grows. you have to document that the patient has autonomous hypersecretion of growth factor. ring size. The adenoma increases in size and the patient bleeds into the adenoma then virtually blows out their pituitary. probably hypopituitarism. neurosurgical consult for transsphenoidal decompression of the tumor. * Treatment for acromegaly is octreotide (somatostatin). * Screening test for hypopituitarism is the insulin-tolerance test. and those are FSH. high GH. done by a glucose tolerance test. * Treatment of Sheehan syndrome is to replace hormones they have lost.66 - . granulomas. The meninges come into the sella and push out the pituitary. Patients usually have a pre-existing pituitary adenoma that was not treated well or not treated at all. So you expect high glucagon. You can check the cortisol level at the same time to see if ACTH is missing too. Then do the MRI looking for the tumor in the pituitary. This is needed to concentrate your urine. high-dose corticosteroids. nuchal rigidity. administer appropriate hormones. * DI patients complain of polyuria and polydipsia. If after glucose load. You can live without these. this is an inappropriate response and we say the patient likely has acromegaly due to autonomous hormone release. Pituitary Disease: Hypopituitarism * Hypopituitarism is loss of pituitary hormones over time. evaluate electrolytes. somatomedins). normal response is increased insulin and decreased counter-regulatory hormones. ACTH which affects the adrenals. LH. You measure growth hormone an hour later and expect it to be elevated.
* When your thyroid puts out T3 + T4. Posm will increase. This sounds like a paradox because the patient is getting rid of lots of urine. strokes. If the patient has no ADH (CDI). * SIADH can occur with medications like vinblastine and vincristine. The diuretics get rid of sodium and help retain water. hypertonic saline can be used. but the aim is to retain water. Correcting hypernatremia too quickly with free water can result in cerebral edema and seizures. At the same time. the patient does not make urine to conserve free water. Treatment of choice is water restriction. but they are putting out dilute urine (Uosm low/not changing). demeclocycline is probably preferred due to less side effects and less drug-drug interactions. The current TSH testing can diagnose hypothyroidism or hyperthyroidism with a 95% confidence interval. These patients do not wake up in the middle of the night to go to the bathroom. * In severe hyponatremia. * Psychogenic polydipsia is characterized by large intakes of water and large outputs of urine. * Test for DI is the water deprivation test. tuberculosis. you will start to see a normalization of Uosm (Uosm increasing and concentrating). * Patients presenting with polyuria and polydipsia either have diabetes mellitus (check serum and urine glucose) then think about DI. Sometimes the sodium is so low we have to treat the SIADH. which increases proximal sodium and water reabsorption. * SIADH can occur with CNS processes like tumors. To suppress TRH and TSH. * Treatment for NDI is hydrochlorothiazide or amiloride. The mechanism for thiazide diuretics is to decrease distal tubular sodium reabsorption. * Syndrome of inappropriate ADH (SIADH) secretion is when patients produce small amounts of concentrated urine. * Patients with DI usually have access to water. and T4/T3 from thyroid. The thyroid produces mostly T4. Water deprivation test will show almost normal response. * Treatment for CDI is to give vasopressin (ADH) or give intranasal desmopressin. Normal is increased Posm and increased Uosm (urine concentrates). To see how the thyroid is really working. so they are very good tests. it has a stronger feedback. These patients hold on to too much free water. * Treatment of SIADH is to treat the primary disease. * If the TSH is normal.Study Notes – Internal Medicine James Lamberg 28Jul2010 receptors in the kidney do not function. but also think about psychogenic polydipsia. so people measured total T4 then got RT3U (resin T3 uptake) to indirectly DO NOT DISTRIBUTE . so diabetes insipidus has dilute urine. which decreases distal delivery of sodium and water. serum Na+ is increasing. T4. not the total because you only care about free T4. Treatment could also include drugs that cause NDI like lithium and demeclocycline. granulomas. and has the feedback effect to TSH and TRH. * Do not assume enlargement or nodules of the thyroid mean hyperthyroidism. * Free T4 use to be a difficult test. COPD. so does nothing to TSH or TRH for feedback nor does it have metabolic effects. A patient with DI cannot do this. * Thyroid levels of control are hypothalamic function (TRH). which decreases extracellular volume. nearly all of it is bound to albumin.67 - . so they can take in 20L and put out 20L. in general that patient is euthyroid. Common scenario is a patient on lithium for many years who goes into the hospital for surgery (or another scenario where water access is lost) and now they become very dehydrated showing with severe hypernatremia. At this point. where plasma osmolality is plotted against urine osmolality. The causes of NDI are lithium and demeclocycline. so as they are getting more dehydrated they will keep putting out dilute urine. In a normal individual will get dehydrated and Posm will increase. which increases urinary excretion. T3. and TSH (indirect measurement). * SIADH can occur with lung processes like abscess. so you give the patient vasopressin (ADH). however you do not have the pressor effects of ADH.1% of the total. When these patients drink lots of water the wash out the medulla of the kidney and lose concentrating capabilities. * T3 is a more potent hormone with a better effect. this can only be NDI since the kidney receptors are not responding to ADH. * Insipid means devoid of characteristic. * The best test for screening for thyroid disease is thyroid stimulating hormone (TSH) as it is the most sensitive and specific test. T4 in the periphery gets converted to T3. and finally decreases urine output. you cannot differentiate CDI from NDI. It is when they lose access to water that they get very dehydrated. The free T4 is less than 0. If you give ADH and there is no change in Uosm. trauma. then SIADH usually resolves. it is metabolically active. Forget about the T4 and forget about the T3. you want free T3 and free T4. Thyroid Function Testing * Thyroid gland produces T4 as the main secretory product. which dilutes the sodium and causes hyponatremia. This is why we need to objectively assess the thyroid by looking at thyroid hormones. This is called thyroid binding globulin and it is an inactive form. infections. Because T3 is more potent. These drugs can make the ADH receptors in the kidney unresponsive to ADH. Do not replace too quickly due to risk of central pontine myelinolysis. Desmopressin is like ADH but only different by one amino acid. This disease runs in families. pituitary (TSH). you would give T3 hormone.
* Complication of PTU and methimazole is agranulocytosis. Since this is an ICU patient. wait 24h. Thyroid hormone is being spilled into the periphery due to destroyed thyroid cells but uptake is low because thyroid is injured. Example is Graves disease. free T4 elevated. Tell them to stop the medication and have their white cells checked. free T4 normal. It is reversible agranulocytosis as long as you catch it. Symptomatic relief includes beta-blocker therapy (propranolol. free T3 elevated. If patient is on this medication and calls you saying they feel horrible and are running a high fever. Anti-thyroid medications are propylthiouracil (PTU) and methimazole to decrease thyroid hormone level. repeat in 48h to see what the uptake is. Give them a little bit of PTU and propranolol to cool down the thyroid.68 - . * Primary hyperthyroidism: TSH low. but TSH came back normal. The cause is an immune process. Anything under this would be hypothyroidism. Thyroid hormones use to be in weight reduction medication a few decades ago even in this country. free T4 elevated. There is no need for endocrine management here. Hyperthyroidism * Graves disease is the most common cause of hyperthyroidism. RAI-uptake scan is low.9% of thyroid hormones are bound to albumin. RAI-uptake scan high. intolerance to heat. Ophthalmopathy is treated separately as patient may not be able to close their eyes and may get eye ulcers. increased FT4. Likely to have abnormal growth hormone.g. Example patient with nephrotic syndrome or cirrhosis. RAIuptake scan low or normal. weight loss. Free T4 in this patient would be normal and TSH would be normal. Within months or years the patient will become hypothyroid. anything over this is hyperthyroidism. * With fluctuations in protein the body will keep the free T3 and free T4 stable. they will get agranulocytosis with that as well. weight loss attempt): TSH low. total protein level is down. Example is hypopituitarism. so you have to follow this patient every six months to check thyroid hormones. then scan the thyroid. free T3 elevated. toxic nodular goiter. * Graves laboratory findings would be low TSH. * Secondary hypothyroidism: TSH low. Radioactive iodine has not been shown to cause cancer. * If agranulocytosis occurs with PTU then you cannot give the patient methimazole. * Proptosis and exophthalmos commonly gets worse when you treat Graves disease. This patient has sick euthyroid syndrome. Is this patient hyperthyroid? No. Radioactive iodine is given to the patient. they have increased proteins so total T4 will increase. then give thyroid medication (synthroid or any other T4 form). * In pregnant patient with Graves disease the only anti-thyroid medication we can use is PTU. and elevated RAI-uptake if you felt you needed it. free T4 low. * Exogenous thyroid medication use (e. they likely have a lot of other comorbid conditions. any changes in albumin and protein levels in the body will fluctuate the total T3 and total T4 levels. atenolol) until patient is out of acute phase meaning they feel better and become euthyroid. Example would be pregnant patient or patient taking estrogen. LH. free T3 normal. Someone thought this patient might have a thyroid problem. * Anti-microsomal antibodies sometimes associated with Hashimoto disease. * Management after acute phase is definitive treatment with radioactive iodine to kill the thyroid. menstrual irregularities. Normal is 1040% uptake just as a note. * Pregnancy or protein-increasing medication: TSH normal.Study Notes – Internal Medicine James Lamberg 28Jul2010 measure free T4 index. * Radioactive iodine uptake scan (RAI-uptake) is a way to directly measure function o the thyroid. * A patient is intubated in the ICU and the patient’s FT4 was high or low. * Management in the acute phase is to relieve symptoms and reduce peripheral thyroid hormone. it is an indirect measure of T4. diarrhea. Example is subacute thyroiditis. free T4 elevated. antibodies act like TSH to rev-up the thyroid. * Since 99. We can also use propranolol. bruit over thyroid. free T4 low. but you definitely DO NOT DISTRIBUTE . Total T3/T4 would be down in this patient but it is not hypothyroid. * Thyroid globulin immunoglobulin sometimes associated with Graves disease. antibodies that affect the TSH thyroid receptors. So they may need surgery. sometimes swelling of the feet (pretibial myxedema). then take the patient to surgery in the second trimester. So we can only use these at low doses. and FSH because usually not just one pituitary hormone missing. Resin T3 uptake does not measure T3. free T3 elevated. treatment is to wait. tachycardia. elevated total T4. RAI-uptake scan is low. So be careful when you see a total T4 or total T3 instead of free T4 or free T3. The thyroid enlargement is diffuse and is the only time in thyroid disease where you get proptosis and exophthalmos. * Thyroiditis: TSH low. palpitations. When they become hypothyroid. Again. this test is not done anymore so look for a free T4 test. Free T4 and TSH would be normal in this patient. Propranolol can cause small for dates. or steroids. tremor. or orbit radiation. This patient should not be treated with antithyroid medication. RAI-uptake scan normal. * Other Graves signs include dermopathy. Both of these cross the placenta and have side effects.
This causes spilling of T4 and T3. Patient is a little puffy and edematous. and steroids because of hydrocortisone dysregulation. transient. and iodide. which looks like Graves disease. course hair. * Hashimoto associated with other autoimmune diseases such as pernicious anemia. you want to give this slowly in the elderly patient who may have coronary heart disease. * Both hyperthyroidism and hypothyroidism cause proximal muscle weakness. warming blankets. aspirin. Biopsy here will show lymphocytic infiltrate. Thyroiditis * Thyroiditis is an inflammatory condition of the thyroid gland and is relatively common. periorbital edema. cholesterol increases due to lack of metabolic hormones. This is a very dangerous dose but it is the only way to treat these patients. * Thyroid storm usually in patients with Graves disease and precipitated by a condition such as infection or surgery. a couple days later they will have more iodide so they can produce much more T3/T4. Hypothyroidism * Most common form of hypothyroidism is Hashimoto thyroiditis. T3. treated with propranolol. * Because subacute thyroiditis is an inflammatory process. also called De Quervain thyroiditis or giant cell thyroiditis. * This is Hashimoto thyroiditis. cold intolerance. Also give fluids. cooling blankets. acute inflammatory markers will be elevated. Inflammatory process can be acute where there is intense inflammation of the thyroid. After a week or month. has constipation. constipation. * Chronic low-grade inflammation of the thyroid will eventually lead to fibrosis and destruction. a type of dementia can form. Iodide is the cornerstone of thyroid storm treatment. * Presentation occurs mostly in elderly patients and they have mainly cardiac manifestation such as atrial fibrillation. * Treatment is thyroid hormone replacement usually in the form of T4. CHF. low FT4. In all severe thyroid problems there is dysregulation of adrenal steroid production. These patients have altered mental status. dry skin. * Iodide buys you some time. conservative management. If you do not manage the thyroid storm patient. Exam shows decreased deep tendon reflexes specifically the relaxation phase. are hypothermic and are sometimes found out in the cold (cold or infection precipitated the untreated hypothyroidism). same process. Thyroid will either output T3/T4 or grab iodide but not generally both. maybe one. * Toxic nodular goiter is more common in adults and older patients. Palpation of the thyroid results in pain. replace thyroid hormone. Subacute thyroiditis is most likely due to a viral infection. * Treatment of myxedema coma is high dose of thyroid hormone. * Symptoms of hypothyroidism include weight gain. Elderly patient may develop chest pain and may even get a myocardial infarction. fibrosis and scaring of the thyroid. * Treatment is propranolol even if they have hypotension. The thyroid eventually dies out and the patient becomes hypothyroid. and steroids (hydrocortisone). which will be low. Toxic goiter means the thyroid goiter produces thyroid hormone. * Treatment is pain medication such as NSAIDs. * Can have antimicrosomal antibodies.69 - . congestive heart failure. * Toxic nodular goiter exam will not show a diffuse enlargement. * Labs for subacute thyroiditis show low TSH with high FT4/FT3. * Post-partum thyroiditis is subacute thyroiditis after delivery. These patients will usually present with hypothyroid symptoms as the thyroid has been destroyed. PTU. start at 25mcg/day then go to 50mcg/day then consider going up if needed. We also give the patient a more potent hormone. For elderly patient. * Treatment for thyroid storm also includes fluids. like T4 at 300mcg. * Elderly patient develops dementia. so these patients usually present with hyperthyroid symptoms. tachycardia. Order the RAIuptake test. so giving the patient iodide will down-regulate the production of T3/T4. * Lab profile is high TSH. and all of a sudden developed high cholesterol. These patients usually had a non-toxic goiter prior. * A normal adult mainstay does is 100mcg/day. low FT3. Since these are metabolic hormones.Study Notes – Internal Medicine James Lamberg 28Jul2010 do not want to give it to a pregnant patient. Remember high doses of T4 given. these patients will become euthyroid. * Treatment is the same as all hypothyroidism. fever. You will find nodules. ESR will be elevated always. maybe many. * Myxedema coma is a severe form of hypothyroidism. This is an immune process where there is production of antibodies and lymphocytes that cause chronic inflammation of the thyroid. starting the process again. hypotension. This is high output cardiac failure. * Iatrogenic hypothyroidism is also common in this country because of how we treat Graves disease. DO NOT DISTRIBUTE . Non-toxic goiter means nothing is being produced from the goiter. * This is subacute thyroiditis. It would rather grab onto iodide. Thyroid Storm * Thyroid storm definition is a hyperthyroid patient with delirium.
* Exception is follicular cells found on FNA. If TSH low the patient has some form of hyperthyroidism so you treat as hyperthyroidism (toxic nodular goiter). If thyroid cancer found on pathology of FNA. look at PO4-. * Papillary cancer is benign. occurs in older individuals. releasing calcium. PTH stimulates osteoclasts to break down bone and release calcium into serum. parathyroid hormone (PTH) increases. Phosphate will always be low. thyroid scan showing cold nodule. surgery then T3 or high dose T4. * PTH also affects the kidney to reabsorb calcium and the intestine to absorb more calcium through vitamin D. * Calcitonin tones down calcium. follow patient but no management needed now. 10yr survival 80-90%. activating osteoclasts. * With high levels of PTH secretion. then you know the patient has a non-functioning thyroid nodule and thus a chance for cancer. * Protocol for thyroid nodule found is to get TSH to see if functioning. Say they have primary hyperparathyroidism with an autonomous adenoma secreting PTH but what if the patient has vitamin D deficiency or renal failure? So calcium in this scenario would be about normal or low if you do not have enough bone mass. If follicular elements are found on FNA. * There is an autonomous adenoma that is producing PTH. But. * Medullary cancer of the thyroid arises from the parafollicular cells (C cells. phosphate trashing hormone. * Treatment of follicular cancer is the same as papillary cancer. * Follicular cancer of the thyroid occurs in older individuals and usually has hematogenous spread. * Other risk factors for thyroid cancer are male gender. This is because you do not know where the patient started with calcium. Hyperparathyroidism * Primary hyperparathyroidism is the most common cause of hypercalcemia and is the most common cause of benign or mild hypercalcemia. Less than 5% of patient live more than a couple of years. * If a scan is done and a warm or hot nodule is found. which also has pheochromocytoma and parathyroid hyperplasia. * Always do a fine needle aspiration on a thyroid nodule. If FNA is benign. one form being solitary medullary cancer. decreases calcium by reducing bone resorption. Mnemonic: PTH. Ca++ is not a sensitive index of parathyroid hormone. What do you do with the thyroid nodule? Every time you have a thyroid nodule the first test and only test to do is a fine needle aspiration (FNA). does not metastasize but it grows focally. If TSH normal.Study Notes – Internal Medicine James Lamberg 28Jul2010 Thyroid Cancer * Papillary cancer of the thyroid is the most common. We can use salmon calcitonin to decrease calcium levels in hypercalcemia. * Vitamin D increases calcium and increases phosphate. no treatment available. * Risk factor for thyroid cancer if you find a lump is radiotherapy to the head and neck (presumed to have cancer until proven otherwise). Think that this is likely follicular cancer. * Medullary cancer also associated with MEN-II (MEN-IIa). The difference between a benign follicular adenoma and follicular cancer is the architecture. * Patient presents with some kind of thyroid cancer and metastatic disease to distal visceral organs. * Anaplastic cancer of the thyroid is deadly. so great prognosis.70 - . It is associated with some familial forms. about 70-80% of all primary thyroid cancer cases. the next step is not waiting. the nodule has to be non-active meaning no hyperthyroidism. so you would need to know that the treatment for that is radiation therapy (XRT) only to the head and neck. Also associated with MEN-III (MEN-IIb). * When talking about PTH affect. the calcium may be high or normal but the phosphate will always be low. usually grows focally and metastases to the lymph nodes around the thyroid. * Iodine scan is a way to monitor these cancers. * Treatment of papillary cancer is surgery then give patient T3 or high doses of T4 because cancers of the thyroid are probably sensitive to TSH so you want to suppress TSH production as much as possible. They may just say the patient had Hodgkin disease stage IA several years ago. associated with radiation to the head and neck area. So you cannot tell from only an FNA. * Hypercalcemia found on routine screening 50% of the time it is primary hyperparathyroidism. do not order a scan of any kind or an ultrasound. Parathyroid Disease * As a patient’s calcium goes down. then do surgery. * You notice in the family that patients have had solitary medullary cancer (not multiple endocrine neoplasia). This prevents hypocalcemia to the point of tetany and death. You have to do the FNA. they can look for metastatic disease. then do thyroid surgery because that is the only way you can tell if this is a cancer or just a benign tumor. * Treatment of papillary cancer allows for 95% of patient to live 5 years. older age. is slow growing. calcitonin producing cells). * When PTH activates the kidney it wastes phosphate (PO4-). associated lymphadenopathy. * Patient usually comes to the office complaining of a thyroid lump or you find one on routine exam. Next step in management is fine needle aspiration. 80% of cases DO NOT DISTRIBUTE . which also has pheochromocytoma and neuromas. recent growth of nodule.
5. then watching the serum calcium go up and down. polydipsia. Treatment here is IV calcium with ECG monitoring for QT abnormalities. When we measure calcium in serum we get total calcium and 40% of this is ionized. Hypocalcemia after surgery for primary hyperparathyroidism is due to calcium going to bone and nothing left to stabilize the calcium.6 = 8. * Most blood assays only check for parathyroid hormone that is intrinsic. So patient goes from hypercalcemia to hypocalcemia. * A patient with nephrotic syndrome would have a lower total calcium. If calcium is still high. Do not write for IVF and furosemide at the same time here. * With one gland hyperplasia. Treat hypercalcemia with fluids (normal saline) primarily. pituitary tumors. * Most of vitamin D is absorbed in the summertime due to sunlight activation. Watch these patients closely in a telemetry unit and monitor calcium levels for a couple of days. * Treatment is surgery for definitive treatment. Hypercalcemia causes shortened QT. polyuria. it should be done in all patients with symptomatic hyperparathyroidism such as kidney stones.2mg/dL) = 2 * 0. make sure to account for low albumin states. Ionized calcium is the part that affects neuromuscular irritability. With vitamin D deficiency and in some stages of chronic renal failure the parathyroid hormone becomes ineffective. osteitis fibrosa cystica. Say nephrotic patient is 2mg/dL albumin and total calcium level is 6. In 15-20% of cases there is four gland hyperplasia or parathyroid cancer. After surgery. * With hypocalcemia. So sarcoid patients develop hypervitaminosis D in the summertime or when they go to sunny areas. so majority is protein bound. * To distinguish in a hypercalcemia patients between primary hyperparathyroidism and hypercalcemia of malignancy. These are breakdown of bone. On the other hand. you order PTH level. For every drop in albumin by a single point there is a drop in calcium of 0. and parathyroid tumors. This is the cause of the hypercalcemia (and more phosphorus too). * Older individual with mild asymptomatic hyperparathyroidism may be watched. Treatment is usually not necessary. Hypercalcemia of Malignancy * Hypercalcemia of malignancy can occur through multiple metastases to bones. * Hypercalcemia of immobilization is also benign. so that is a case when you could give calcitonin at the same time as a bisphosphonate. * Hypocalcemia prolongs the QT interval. but their ionized calcium would remain the same. wears off after 48hrs) or bisphosphonates (long acting) like pamidronate. * Hypercalcemia associated with cancer is usually severe. Diffuse granulomas seem to activate vitamin D. you have three glands that are not working well.71 - . * Mild hypercalcemia would be bone pain. such as multiple myeloma. So 6. * Normal albumin is 4mg/dL. this may be due to a gastrin producing pancreatic tumor (Zollinger-Ellison) with parathyroid tumor.5 + 1. hydrochlorothiazide retains calcium. which activates the osteoclast. DO NOT DISTRIBUTE .6. They will have an elevated calcium level and it is not likely cancer or hyperparathyroidism. * Fibrosa cystica (brown tumors) develops in the bone due to the constant osteoclast activation resulting in cyst formation. so hypervitaminosis D. Hypocalcemia * Whenever you see hypocalcemia. Fluids is the cornerstone of treatment for hypercalcemia. This would be a nursing home patient who is in bed most of the time. Severe hypercalcemia occurs with > 15mg/dL and is a medical emergency. The other mechanism is through production of PTH-like molecule. * Primary hyperparathyroidism associated with MEN-I (the 3 Ps): pancreatic tumors. * Furosemide and diuretics can be seen in hypercalcemia protocols because furosemide gets rid of calcium. So PTH-like substance may not be picked up by parathyroid hormone levels. PTH level would be elevated only in primary hyperparathyroidism. the other three glands shrink due to negative feedback with calcium. What is this patient’s real total calcium? Answer is (4mg/dL . A patient who got exploratory surgery around the neck area could have had damage to parathyroid gland circulation. this is called hungry bone syndrome. Patient has hypercalcemia with severe peptic ulcer disease and diarrhea. It is a chronic granulomatous disease. think about hypoparathyroidism.Study Notes – Internal Medicine James Lamberg 28Jul2010 there is a single adenoma. giving diuretics if calcium is high or if kidney stones occur uncommon. Furosemide does not do much to the calcium level. it is given because the mainstay of treatment is fluids and we do not want to cause fluid overload in an elderly patient. These patients hardly ever have symptoms. only give furosemide if evidence of overload. then calcitonin (immediate action. * Familial hypocalciuric hypercalcemia is a benign disorder. * Four gland hyperplasia requires removing all four glands. Treatment is just to monitor the patient. where granulomas occur mainly in the lung but can occur anywhere. Lab would be low phosphate. abdominal pain.1 total calcium. Squamous cell cancer does not metastasize much.8 factor = +1. no need for medications or further testing. * Sarcoidosis can cause hypercalcemia. putting one in the arm. Example is squamous cell lung cancer or esophageal cancer.8. it grows focally.
This results from an inflammatory process of the pancreas beta cells causing them to get destroyed and leading to insulin deficiency. * Type II diabetics can develop hyperosmolar hyperglycemia nonketonic syndrome (HHNS). After many years. Maybe a couple of weeks. After time. This leads to tertiary hyperparathyroidism. Some people mistakenly think Type I DM is congenital because patients present as children. * Definition of diabetes is fasting glucose > 126 for two consecutive visits. Magnesium is needed to secrete PTH and is needed for PTH to act on the osteoclast and the kidney. you just have to control the patient’s sugar. These patients need laser treatment to the eyes or they will go blind. These patients do hot have any of the microvascular complications. but non-insulin dependent diabetes mellitus (NIDDM). Rickets. They do have severe dehydration.g. usually older individuals. Resistance to insulin decreases with weight loss. You cannot reverse the peripheral vascular disease or cardiovascular complications. * Identical twins with Type I diabetes has only about a 50% concordance rate. * A Type I diabetic who presents at your office has not had the disease for very long. you diagnose them with diabetes. If that does not work you do oral hypoglycemics (e. You check their glucose and find it to be elevated. So patient with DM must DO NOT DISTRIBUTE . severe dehydration. Calcium may normalize in the beginning. but remember there is not much family link here.Study Notes – Internal Medicine James Lamberg 28Jul2010 * Any drop in magnesium levels affects parathyroid hormone. they develop these at least 5 years later. Diabetes Mellitus * Diabetes is a disease of carbohydrate metabolism. * Type I diabetics are insulin dependent. * Hyperosmolar hyperglycemia nonketonic syndrome (HHNS) is a state of high sugars. metformin). It is seen in vitamin D deficiency. Most patients present complaining of polydipsia and polyuria. not the macrovascular complications. * Diabetic retinopathy is the most common cause of blindness in middle aged people. * DKA usually occurs in young patients with no other comorbid diseases. so these patients can break down lipids as their main form of energy which produces ketone bodies and diabetic ketoacidosis. * Symptoms of latent tetany include Chovstek sign where you tap the facial nerve and see an ipsilateral facial twitch. Proliferative retinopathy is neovascularization. they become autonomous. but that’s probably years later. * Vitamin D deficiency (secondary hyperparathyroidism) would cause low calcium and low phosphate. * Secondary hyperparathyroidism is caused by hypocalcemia. * Studies show that even excellent primary care physicians miss proliferative retinopathy. * We can only reverse the microvascular complications of diabetes with tight glycemic control. kidney (nephropathy). You cannot live without insulin for a long time. Now you cannot suppress the calcium and you have to remove the parathyroid glands. the new vessels are prone to bursting and bleeding which leads to blindness. but they do have diabetes. Ketosis can occur because there is no insulin. usually 30-40+ years of age. This patient would need to go to the ophthalmologist right away to look for retinopathy. * A Type II diabetic presenting at your office will have complications already because they have had the disease for at least 5 years or more. HHNS can progress to hyperosmolar coma. This has a worse prognosis than diabetic ketoacidosis (DKA) because it occurs in older individuals with comorbid conditions. If that does not work you use insulin. For background retinopathy. * Type II diabetics are overweight. The types of microvascular complications are the eye (retinopathy). Patient could get laryngospasm. parathyroidectomy. so PTH increase and PO4. * Identical twins with Type II diabetes has a 100% concordance rate. brain (neuropathy).72 - . You do not have to treat the patient right away. * Type II diabetics are insulin resistant. renal insufficiency. Background retinopathy is associated with retinal hemorrhages and cotton wool spots on fundoscopic exam. you would need to look that day for proteinuria. Presentation is usually diabetic ketoacidosis. no acidosis. or the Trousseau sign where you put a cuff on the patient’s arm then inflate the cuff and leave it there for a minute or so until you see tetany (can be rather dramatic). It usually does not cause blindness. and decide if they need an ACE-I. the parathyroid glands start acting autonomously which leads to tertiary hyperparathyroidism. but no acidosis. * Renal failure patient can get secondary hyperparathyroidism due to lack of calcium. Type I diabetes is usually seen in young individuals. It is difficult to study type II DM because patients have had the disease for a long time but do not know it. * Treatment of hypocalcemia is oral calcium +/. * With secondary hyperparathyroidism. * If patient presents in HHNS or DKA. * Initial management is diet modification. patient is usually slender and no family history of diabetes.decreases.vitamin D if no symptoms and IV calcium if symptomatic. it runs in the family unlike Type I. the parathyroid glands get activated to constantly dump PTH. These patients may have glucose levels in the 1000s. * Renal failure or hypoparathyroidism would cause low calcium and high phosphate.
first line drug is ACE-I. * Do not diagnose diabetes with an HgA1c level. this is random. Which insulin will you increase to cover this (NPH. then the counter-regulatory hormones kick in and by the time the patient wakes up they are hyperglycemic. AM v PM)? Increase AM regular insulin. 8am sugar is 300. midnight sugar of 120. During the night you see this example. Now what do you increase? Increase AM NPH insulin. * Type II DM can get a little NPH once a day or so. What happens is the insulin wears off at night leading to hypoglycemia. feels full after eating very little. then they develop clinical diabetes. patient feels bloated. The mass decreases until a diabetic threshold is reached. * Exception is patient with high sugar in the morning. lisinopril). nephropathy) do tight glycemic control. give the patient AM regular and NPH. decrease the amount of insulin at night until you can figure out if this is the dawn effect or this is the somogyi effect. their insulin needs get DO NOT DISTRIBUTE . Patient will say they are not sleeping well or they are having bad nightmares.73 - . it is just a monitor of disease activity. Say patient has blood sugar just before dinner is around 300. Break that down into taking most of the insulin in the morning and about 1/3 at night. you give 66 units at the next AM and 33 units at next PM. When you decrease the night insulin. It does not matter what the patient tells you about their control or their blood sugar at the office visit. * Autonomic neuropathy in DM is associated with gastroparesis. Called “law of 2/3rds”. * A normal blood sugar (< 125) over time would correlated to an HgA1c of < 7 or even < 6. If patient gets an infection. like stress or a cardiac event. If patient used 100U over the last 24h prior to hospital discharge. so that will kick in around lunch time when given in the AM. Say patient comes in saying their noon blood sugar check is around 300. neuropathy.5. has diarrhea. wrist drop. * HgA1c of 7. Now you increase the PM regular insulin. * Patient with diabetes usually presents because diabetes is precipitated by something. * To cover a patient throughout the day. use 2/3 NPH and 1/3 of regular or maybe 1/2 of each. If you increased the insulin in this patient at night. the somogyi effect or somogyi phenomenon. Another option is to have the patient wake up at 3am a couple of nights to check their blood sugars. * HgA1c of 8+ correlates to sugars running above 200. use 2/3 NPH and 1/3 of regular (so of the 66. * Type I diabetes occurs due to an inflammatory process. If you put the patient on ACE-I. you could put them in a coma. This looks at sugar over 2-4 months. * Peripheral neuropathy in DM is the stocking and glove distribution (loss of sensation). So patient may get regular insulin then NPH insulin in the morning. * With morning hypoglycemia. there is a decrease in functional pancreatic mass after insulitis event.5 correlates to sugars between 150 and 175. The problem is the second scenario with morning hyperglycemia. Autonomic neuropathy also causes erectile dysfunction and hypotension. or cranial nerve abnormality. Type I diabetic patient usually have an infection. Any patient with hypertension and diabetes. Somogyi effect is due to rebound from too much insulin use. 3am sugar of 70 (hypoglycemia). * Patients may have complications but show up at your office with normal sugars. NPH onset is around 6-8 hours so it will kick in later in the afternoon. So this is assumed to be from a viral infection (e. So the treatment of proteinuria or microproteinuria in a DM patient is ACE-inhibitor (e. * Regular has a peak action of 2-4 hours. Type II diabetic patient may have infection or cardiac event. coxsackievirus) in predisposed individuals. Type I DM need insulin twice a day. 44 NPH and 22 regular insulin). To fix this. The bottom line is an HgA1c over 8 means they have been poorly controlled for the past few months.Study Notes – Internal Medicine James Lamberg 28Jul2010 go to the ophthalmologist at least once a year. To measure glucose control over time. In the AM. * Nephropathy in DM causes nephrotic range proteinuria > 3g/day but not nephrotic syndrome. but they do not wake up from the hypoglycemia. 5am sugar is 90. * Treatment of Type I DM is insulin.g. This can be true high sugar because insulin you gave the day before has worn off. Meaning get to normal blood sugar which is < 125. give some rapid insulin and some intermediate acting insulin. Say glucose before bedtime is in the 300s. the patient with somogyi effect will have normal sugars in the AM but the patient with dawn effect will have even higher sugars. Just understand that a type I diabetic will need coverage throughout the day with short-acting insulin and intermediate-acting insulin. followed by regular insulin and NPH at night. * Determination of insulin units is based on what they used in the past 24 hours. look at the glycosylated hemoglobin (HgA1c). * To stabilize any of these complications (ophthalmopathy. The longer nerve CN VI gets affected in many lesions but in diabetes for reasons unknown CN III is the most commonly affected. this is called the dawn effect. be worried about somogyi effect and do not increase the night insulin.g. Central cranial nerve that is most affected in diabetes is CN III (ptosis). * Mononeuropathy in DM would be a patient with foot drop. regular. you will decrease the amount of protein in the kidney. Yes. In the PM. First. * Type I DM. Then give them regular before dinner and NPH before bedtime to carry over until the morning.
They come with clinical evidence of diabetes. UTI) and diabetes is started. DO NOT DISTRIBUTE . * Treatment during the honeymoon period is to give the patient low dose insulin.exenatide or insulin or glitazone. then insulin likely needed 10 years later. Treatment of the infection (e. * Sulfonylureas include glyburide. glipizide. Another complication that can occur with exogenous insulin takers is development of insulin antibodies. They act on the beta cells to produce insulin. patients have less complications and do better on this medication. they will have high insulin and high C-peptide because the only way you can secrete endogenous insulin is to co-secrete with C-peptide.sulfonylurea. If the patient has an insulinoma. It also facilitates the movement of glucose into muscle. * Glipizide and glyburide are given once a day or maybe twice a day. They start working out in the evening before dinner.74 - . or more commonly the patient is taking exogenous insulin.metformin or sulfonylurea. Hypoglycemia * Hypoglycemia is not just low sugar in the blood. * Acarbose and miglitol are alpha-glucosidase inhibitors that are rarely used because of the severity of their sideeffects (flatulence and bloating). Patient is taking regular + NPH in the morning and evening. stop the metformin at least 24h ahead of time. you can watch and give sugar then discharge. frequent meals. * Type 2 DM (Asians): glitazone. Patient taking exogenous insulin will have high insulin level but low C-peptide. and troglitazone are thiazolidinediones (TZDs) which improve glucose use by cells. It also blocks. This is called the honeymoon period. this is an appropriate response to not eating. tolbutamide. symptoms consistent with hypoglycemia. pioglitazone. * Type 2 DM (non-obese): sulfonylurea or metformin first. and glucagon. so in an overdose you should anticipate hypoglycemia for 24 hours and admit to the hospital. * Metformin is a biguanides and does not affect the beta cells. If you cause a little renal failure with the dye you could increase the lactic acidosis side-effect seen with metformin. If you measure insulin during hypoglycemia and it is normal or high. Tell the patient to keep exercising and then decrease the morning NPH insulin. chlorpropamide. but notice they feel dizzy and their sugars run in the 50s. That is because they have residual pancreatic mass and non-clinical diabetes. They also sensitize the peripheral cells to the effects of insulin. * Rosiglitazone. So check creatinine to rule out renal insufficiency if DM patient develops hypoglycemia. a little. then metformin. * Type II DM treatment starts with diet. glucose uptake from the gut. lactic acidosis (reason to discontinue medication) which occurs more commonly in patients with renal insufficiency * When sending a diabetic patient for a radiologic study that needs IV contrast dye. Oral Hypoglycemic Agents * Sulfonylurea have been around for many years. All the sulfonylurea drugs are metabolized by the kidney except tolbutamide. So in a patient with renal failure (common in DM) choose tolbutamide. not insulin has a longer half-life and patient develops hypoglycemia. * Endogenous insulin is secreted with C-peptide at an almost 1:1 ratio. Major action is stopping glucogenesis in the liver. then they call you two weeks later because their sugar level is normal.Study Notes – Internal Medicine James Lamberg 28Jul2010 higher and their pancreatic mass is stressed. so it stops the liver from making sugar. then +/.exenatide or insulin or glitazone.g. pneumonia. improvement after glucose given. * Hypoglycemia with DM cause occur due to exercise because there is enhanced glucose uptake by muscles without insulin. * DM patient develops new onset renal failure. * Hypoglycemia with high insulin is due to a rare pancreatic insulinoma. then switch to simple insulin regimen. Tolbutamide is not used often because dosing is three times a day. growth hormone. By treating this patient you are protecting the residual functional pancreatic mass and not stressing it. * Type 2 DM (elderly): low dose secretagogue. * Type 2 DM (obese): metformin first. which is an autonomous insulin-secreting tumor. * Metformin is a good drug. If you measure insulin and it is zero. then +/. * Normal response of the body to hypoglycemia is to drop insulin down and increase counter-regulatory hormones like cortisol. this is an inappropriate response. * Most sulfonylureas have a prolonged effect. then +/. Treatment is to eat. Example would be rounding in the AM post-call and someone starts to get wobbly. then oral hypoglycemics. * Hypoglycemia in a non-diabetic is initially managed by looking at the body response. The usual profile of the exogenous insulin taker is someone in the medical profession or lives with someone who is diabetic. If patient takes too much regular insulin. then +/. Metformin acts on the liver to stop neoglycogenesis. * Whipple triad: low sugar. They are not used due to their side-effect profiles. then sulfonylurea or insulin or exenatide. there must also be symptoms. Complications of metformin include GI upset and diarrhea (most common).
Obese patients will have abnormal tests. If elevated free cortisol. Yes it can cause a buffalo hump. * Follow-up test is urine 24h free cortisol. It is like the sedimentation rate in temporal arteritis. It is a good screening test because it is done easily and all patients with some form of Cushing syndrome will have an abnormal test (very sensitive. * So if you see a thin person with hyperpigmentation. cachectic because of the lung cancer. pituitary). Next step is get a CT scan or MRI of the pituitary and get neurosurgeon involved. * Dexamethasone is a potent type of cortisol. nodules in the adrenals that mean nothing. Now localize the cause (pituitary. do not assume Addison disease. * Likely the most common cause of Cushing syndrome is iatrogenic. * High-dose dexamethasone suppression test is abnormal. The main function of aldosterone is to keep salt in vessels. and potassium. The difference you know is that patients with lung Cushing have high ACTH with hyperpigmentation and adrenal Cushing do not have high ACTH. Cushing Syndrome * Excess exogenous cortisol does a lot of things but it depends on how long you are taking the cortisol for. maintain vascular tone. Abnormal response is to give 1mg dexamethasone at night then patient wakes up with high cortisol. which peaks in the morning. This is a malignant disease. this patient has some form of Cushing syndrome. causing hypertension. in fact they are co-secreted. So a normal response is suppressed AM cortisol. These patients look thin. it could be Cushing or something else. hydrogen ions. * What if a patient took exogenous sulfonylurea medications? These act on the beta cells to increase insulin and make sugar plummet. diabetes because it is a counter-regulatory hormone. nodules in the pituitary that mean nothing. If there is clinical suspicious for exogenous sulfonylurea use (patient in medical profession or diabetics in family) then check the urine for sulfonylurea levels. even normal people can have abnormal tests. * High-dose dexamethasone suppression test is normal (cortisol suppressed) if pituitary adenoma. causing high levels of aldosterone.Study Notes – Internal Medicine James Lamberg 28Jul2010 * It is important to differentiate exogenous insulin taking from insulinoma. looking just like an insulinoma. Overnight corticotropin releasing hormone (CRH) causes ACTH to increase cortisol. * Small cell (oat cell) cancer in the lung can cause ectopic ACTH secretion leading to Cushing syndrome. lung. then localize. At the DO NOT DISTRIBUTE . psychosis. If you give a patient dexamethasone at night. This is a benign disease in that it occurs over a long time (e. or adrenal). 10 years) before it is diagnosed. now check ACTH and if elevated assume lung cancer.g.g. It is also called Cushing disease because it was in the original patient described (moon facies. buffalo hump. Next most common is autonomous ACTH adenoma in the pituitary. This is likely unresectable. no Cushing. it could be dispersed cells in the pancreas. Next step would be CT scan of the chest. When you measure hydrocortisone in the morning. you can exclude Cushing. After diagnosis.75 - . * Adrenal adenoma or adrenal hyperplasia or adrenal cancer will cause a secretion of cortisol. but not specific). * If dexamethasone suppression test is abnormal. normal response is to see that enough cortisol is present and not release CRH and ACTH. The ACTH is suppressed. to the point where surgery could involve cutting off pieces of the pancreas until the sugar normalizes. due to very high levels of ACTH. and deals with bicarbonate. C-peptide would be elevated as well. This form is autonomous so does not get suppressed. ACTH is similar to melanocyte stimulating hormone. hypertension due to mineralocorticoid effect. * Diagnosis of Cushing syndrome should not involve scanning the patient. If ACTH is low. First screening test is the overnight dexamethasone suppression test. This autonomous secretion cannot be suppressed no matter what you do. Hyperaldosteronism * Conn disease (rare) is caused by an adenoma in the mineralocorticoid apparatus. thus these patients do not have hyperpigmentation. * Autonomous adenoma in the pituitary secreting ACTH can cause Cushing syndrome. If cortisol is normal. It is never used as a screening test because you miss all of the semi-autonomous causes (e. * High-dose dexamethasone suppression test is abnormal (cortisol elevated still) now you are stuck. * First question is to ask if the patient has Cushing syndrome. you do not pick dexamethasone up on the assay. they will be very hyperpigmented. Because of the huge ACTH secretion. purple striae). There is a possibility of excision here. purple striae. if the sed rate is normal then the patient does not have temporal arteritis. It may not be a tumor. * High-dose dexamethasone suppression test is used for localization. wasted. Check that they do not have a form of Cushing syndrome. If the test is normal. Patients with stress. This patient does not have enough time to develop the typical Cushing appearance. Surgery is curative. then adrenal lesion is likely so get CT scan of MRI of abdomen and adrenals. Example would be steroid-dependent asthma or collagen vascular disease. An insulinoma may be very difficult to locate. * Autonomous aldosterone is secreted and aldosterone holds onto sodium (high Na+). It could be either lung or adrenal. You will likely find nodules in the lung that are not cancerous.
which is converted to aldosterone. This is probably the only time you can get random cortisol levels. diarrhea. * If a CHF patient is on furosemide and gets hypokalemia with metabolic alkalosis. Think about secondary aldosteronism from surreptitious vomiting or use of diuretics to lose weight. cirrhosis). hypokalemia. over-diuresis. Adrenal Insufficiency * Most cases of adrenal insufficiency are due to tuberculosis worldwide. * Electrolyte problems are hyperkalemia. causing an increase in 17-hydroxyprogesterone. * Primary hyperaldosteronism (Conn syndrome) is a rare form of secondary hypertension. potassium and hydrogen ions are lost leading to hypokalemic metabolic alkalosis. hyponatremia with hypotension. * Gitelman syndrome is a rare inherited defect in the distal convoluted tubule of the kidneys. vomiting. is that primary aldosteronism has mainly diastolic hypertension and secondary aldosteronism does not have hypertension. So you are over-diuresing that patient. It causes the kidneys to pass sodium. * Diagnostic testing is to activate the adrenals by giving ACTH. Treatment is to cut the diuretic dose. * Treatment is to give mineralocorticoids like hydrocortisone and fludrocortisone because hydrocortisone does not have enough mineralocorticoid action. The low hydrogen ions leaves bicarbonate unopposed. Bartter syndrome is a rare inherited defect in the thick ascending limb of the loop of Henle. very rare. This occurs in 1 of 100 cases of 21-hydroxylase deficiency. The only difference. In the United States. and elevation is eosinophils in serum for unknown reason. These patients have salt-losing nephropathy due to lack of aldosterone. magnesium. 1hr. females are recognized early. but they do not. There is a block in the conversion of progesterone to aldosterone. These are both forms of secondary aldosteronism. It is also called reninindependent aldosteronism. Thus everything gets shifted to the sex hormone pathway. and sex hormones. Males have normal genitalia and can be missed. cortisol. Think about this as a cause if a hypertensive patient complains of weakness and headaches. * You would think the patient with increased intravascular volume would have edema.Study Notes – Internal Medicine James Lamberg 28Jul2010 same time. There is an unknown escape mechanism where the excess water gets wasted. It starts with decreased intravascular volume due to hypotension. * All females born with 21-hydroxylase deficiency have ambiguous genitalia (e. it will not get to normal especially in the edematous states. rather than allowing it to be resorbed into the bloodstream. metabolic acidosis. chloride. * Rapid ACTH test is negative (no increase in cortisol with ACTH given). * Exception for rapid ACTH test is sick patient (stressed). evidence of virilization. Treatment is to replace missing hormones. * In this process. cliteromegaly). Congenital Adrenal Hyperplasia * Cholesterol is converted to progesterone. Give DO NOT DISTRIBUTE . no edematous states. potassium is wasted (low K+) and hydrogen ions are wasted (metabolic alkalosis). If the adrenal is normal. The depleted intravascular volume goes back to the renin apparatus. Thus. 2hrs. * Young woman presents with hypokalemia. Edema is not seen in primary aldosteronism.76 - . * Primary and secondary aldosteronism both have muscle weakness. the rapid ACTH test will likely be abnormal so you can get diagnosis there too. * The most common form of hyperaldosteronism is secondary aldosteronism. then you can get random cortisol levels. but it won’t stop because it is an autonomous adenoma. metabolic alkalosis. So these patients will complain of weakness. But. the rapid ACTH test. which cranks up the aldosterone. The renin apparatus read this and cranks up the renin. Removal of the tumor is curative of the disease and treats the blood pressure as well. and potassium into the urine. most cases are due to idiopathic or autoimmune. etc. patient produces some aldosterone and only has symptoms during stress. Measure cortisol levels at zero. no hypertension. The increased sodium increases intravascular volume (high BP) and this feeds back to renin apparatus which shuts off and tries to tell the aldosterone to stop. It is most common in young adult men. give hydrocortisone 10-20mg/day plus fludrocortisone sometimes for mineralocorticoid action. loss of mineralocorticoids causes low blood pressure. Signs include hypotension and dehydration. Even if the cause is in the pituitary. and some physicians even question this. edematous states (CHF. you know you are causing secondary aldosteronism. Patients with congenital adrenal hyperplasia are missing enzymes to convert progesterone to aldosterone or cortisol. * 21-hydroxylase deficiency accounts for 90% of congenital adrenal hyperplasia cases and is the only one that could be diagnosed in an adult. Also known as renin-dependent aldosteronism. Edema is seen in secondary aldosteronism if they are in the edematous states and not seen in other states. Infections with MAI or CMV in HIV patients can cause adrenal insufficiency. * Adrenal insufficiency causes increased ACTH so there is hyperpigmentation. metabolic alkalosis. * Non-classic form of 21-hydroxylase deficiency can occur.g. The aldosterone increases sodium in an attempt to get intravascular volume to normal. you should see gradually increasing cortisol levels.
10% in children. * Rule of 10% for pheochromocytomas: 10% of patients are bilateral. is associated with the symptoms of fatigue. * Chromosomes are XXY or XXXY. -------------------------------------------------------------------------------------------------------------------------------------------Kaplan Videos (2001) – Hematology/Oncology with Dr. high FSH and LH. thus not the classic presentation. The patients blood pressure goes up. but surgical correction of the underlying disease cures the disease and the hypertension. * Only after you find urine free catecholamines do you proceed to the abdominal CT/MRI. If you take random people off the street you will find 15-20% have some non-functional adenoma of the adrenal glands.Study Notes – Internal Medicine James Lamberg 28Jul2010 enough to maintain the blood pressure and electrolytes at normal. and there is orthostasis despite the hypertension. What do you do next? This is likely an incidentaloma because BP is normal. confusion. Conrad Fischer. Hypogonadism * Kallmann syndrome is isolated gonadotropin deficiency. lightheadedness. * Hct 20-25 symptoms are shortness of breath on exertion (dyspnea) due to lack of oxygen carrying capacity. shortness of breath. Symptoms are most dependent on the severity of the anemia. then increase the maintenance hydrocortisone dose. * Patient presents with high blood pressure and you start them on a medication like HCTZ or beta-blocker. these are called incidentalomas. XXXY has more abnormalities. This is due to a decrease in the release of LHRH. increase maybe up to ten times dose. Cause of death is myocardial infarction. eunuchoid features (large waist). increase hydrocortisone two times dose. hypogonadotropic hypogonadism. This occurs in about 1 in 400-500 births. * Adrenal insufficiency patient going for surgery or gets a febrile illness. A tumor is found in the adrenal gland. Symptoms are dependent on the patient too. MD -------------------------------------------------------------------------------------------------------------------------------------------Anemia * Anemia. * LHRH causes the release of FSH and LH. but the receptors for testosterone production are deficient. 10% extra-adrenal. * Treatment is first suppress epi/norepi by giving alpha-blockade. * Treatment is synthetic LHRH to normalize testosterone. * Treatment is testosterone. which makes testosterone. The patient’s blood pressure is normal. * Patients have normal LHRH. Take an older patient with vascular stenosis. * Hct > 30-35 is usually asymptomatic. and anosmia. Consider pheochromocytoma when patient is young. Older test is VMA (vanillylmandelic acid) and metanephrines. confusion. Severe illness like pneumonia. * Hct < 15-20 is associated with death. * Treatment of pheochromocytoma is surgery. * Most patients (60%) have stable chronic hypertension with pheochromocytoma. regardless of etiology. malaise. Hct 25-30 symptoms are fatigue. do nothing. * Hct 15-20 symptoms are lightheadedness. E. Pheochromocytoma * Pheochromocytoma is a form of secondary hypertension (also primary aldosteronism and renal artery stenosis). patient is 200/110 laying down. 10% are malignant. * A patient gets a CT scan for suspected appendicitis.g. Only if the alpha blockade is adequately controlling the blood pressure could you add a beta-blocker to control symptoms. * Treatment before surgery also includes IV fluids because they are volume depleted. But if you go in and start playing with pheochromocytoma you will get a large norepinephrine and epinephrine surge. Medications include phenoxybenzamine and phentolamine (reversible). * Klinefelter syndrome patients have a 20x greater risk of breast cancer.77 - . This would be expected in pheochromocytoma since alpha receptors are open. increase to 75-200mg/day hydrocortisone. * Diagnostic test is urine free catecholamines. you are using a lot of medication to control their blood pressure. 150/90 sitting up. Do not send an incidentaloma to surgery. * These patients present with small testes. * Treatment is surgical excision after blood pressure normalized with alpha blockade. Key feature is anosmia (lack of smell). * Some patients complain of symptoms like palpitations even with alpha blockade. * Young healthy patient might not die until Hct of 10-12. not high output cardiac failure. Patient could have complications or even die from this. * Pheochromocytoma arises from the adrenal medulla causing increased levels of epinephrine and norepinephrine. malaise. they may die at an Hct of 24 or become symptomatic at 28. These patients are volume depleted for unknown reasons. If major surgery. * High output cardiac failure takes months to develop and is not common in the United States since the precursor DO NOT DISTRIBUTE . * Secondary hypertension is less than 5% of all hypertensive patients. 10% re-occur. If febrile illness. Do not use any other drug except alpha blocker as the first choice or else you leave the alpha receptors unopposed and the patient will have a hypertensive emergency. * Klinefelter syndrome is the most common cause of hypogonadism. syncope.
but the new cells will be more deficient than the old cells. Yep. or normocytic. * Thalassemia anemia: normal iron studies. * To have AML. sideroblastic. coronary artery stenosis (decreased oxygen delivery). low TIBC. Electrophoresis tells you what type of thalassemia. * Macrocytic anemia: B12 deficiency. high is macrocytic. say you get hemochromatosis from iron overload with iron deposits in organs (liver. Hg F is two alpha chains plus two gamma chains. * Left ventricle cannot distinguish between anemia (decreased oxygen delivery). * Microcytic anemia (TICS): thalassemia. If low it is microcytic. Associated with lead poisoning. * Unit packed RBCs has 1mg/mL of iron. Hct is 28. high TIBC. and refractory anemia with excessive blasts are all the same disease.g. zidovudine. heart. Microcytic Anemia * Iron deficiency anemia is usually from blood loss. * Iron deficiency anemia: low ferritin (most specific).g. Most sensitive test is bone marrow looking for stainable iron stores. peripheral neuropathy. pancreas. * Treatment of iron overload in thalassemia major is deferoxamine. fibrocystic breasts. What do you do first to establish a diagnosis? Answer is peripheral smear. 5-6mg/day when pregnant. * Sideroblastic anemia: high iron (only microcytic anemia with a high circulating iron level). and carbon monoxide poisoning (decreased oxygen delivery). * Stroke is also not the cause of death in anemia. Hg A2 is two alpha chains plus two delta chains. liver disease (liver cannot metabolize fats/lipids and they stick to the RBCs). 23mg/day when menstruating. Hg A is two alpha chains plus two beta chains. medications (e. which helps you determine the etiology. these are myelodysplasia with a certain percentage of blasts. iron running out. mercaptopurine). chronic disease anemia. it just means tell the patient to avoid having sex with people who has the same genetic problems that they have (e. so treatment with vitamin B6 can help them. Single gene deletion patients are normal so not likely to be seen in clinic. Macrocytic Anemia * 72yo alcoholic man is brought to you by his son because the man is having memory loss and some numbness and tingling of the feet.g. * Most normal iron loss is through the GI tract. So in alpha thalassemia there are no beta chains. Half the volume of stool is cells. * Ferritin is the storage form of iron. cervix) is premalignant. What is the next step? Answer is look at cell size (MCV). thus is the most common drug cause of macrocytic anemia. Myelodysplasia (MDS) is premalignant for leukemia (AML). Genetic counseling does not mean do all the karyotype testing. These will all look hypochromic and microcytic on peripheral smear. * Hematocrit (Hct) is found to be low. RDW will be increased because the newer cells are smaller. * Thalassemia major requires a unit of cells every 2-4 weeks. myopathy. Total iron binding capacity (TIBC) is unoccupied sites. so you will continue to have bowel movements even if you do not eat. benign prostatic hypertrophy) is not premalignant. Hereditary deficiency in pyridoxine metabolisms. you can live by being stupid and in love but not intelligent with no love. Unit packed cells of 350mL is enough iron for a year. You can live without your brain functioning but cannot live without your heart functioning. Who cares though. it comes down to hypochromic microcytic anemia with normal iron studies. * Latest and greatest treatment for iron deficiency anemia is iron. * Alcohol directly suppresses bone marrow. Four gene deletion patients are dead. * Latest and greatest treatment for anemia of chronic disease is to treat the chronic disease. Hyperplasia (e. thus increased A2 and F. chronic myelomonocytic anemia. If the smear is abnormal showing DO NOT DISTRIBUTE . refractory anemia with ringed sideroblasts. * Treatment of thalassemia minor (thalassemia trait) is do nothing.78 - . family planning). You could treat hereditary hemochromatosis or polycythemia vera with phlebotomy. * Normocytic anemia: hemolysis. Reticulocytes are usually larger. cardiomyopathy. MCV is 110 (normal 80-100). Refractory anemia. skin. colon polyps. folate deficiency. iron deficiency anemia. methotrexate. * Treatment for thalassemia major is blood transfusion every few weeks. There is no real mechanism to get rid of excess iron. these symptoms are from alcohol. So one little mL contains all the iron you need for a day. We cannot treat this form of hemochromatosis (secondary to thalassemia major) with phlebotomy.Study Notes – Internal Medicine James Lamberg 28Jul2010 causes are usually managed. Alcohol can also cause dementia. genetic counseling. blood loss. You only need 1mg/day of iron when not menstruating. but this is not the first test. If the smear is normal. * Dysplasia (e. * Anemia of chronic disease: high ferritin. * Next step in management is iron studies. Two gene deletion is mild anemia and three gene deletion is moderate anemia. Maximum absorbable is 3-4mg/day.g. * Mean corpuscular volume (MCV) tells you the size of the RBCs. alcohol. There are about 5mL in a teaspoon and 15mL in a tablespoon. you need 30% blasts. testicles).
liver disease. * Folate treatment can fix the hematological problem of B12 deficiency. and antibiotics. * Heterozygote sickle cell patients are about 40-50% sickle hemoglobin and 50-60% normal hemoglobin. pain medication. * We know that hypoxia. “painful sickle crisis. most common pernicious anemia. and pain medications. fluids. glucose 6 phosphate dehydrogenase (G6PD). Treatment of B12 deficiency is B12. CBC.6F. and priapism due to infarction by sickle cells of the prostatic plexus of veins that drain the penis. You could see that in tumor lysis. no gallstone history (bilirubin).” His temperature is 98. How do you treat this patient now? Treatment is exchange transfusion. * All present with high LDH but this is nonspecific and increased in anything that causes cell destruction. He says there is no test to disprove pain and that you cannot prove he is not feeling horrible pain. Posterior columns also contain large two-point discrimination pain fibers. Peripheral smear is what you do for this patient. hereditary spherocytosis. as he states. look for normocytic anemia. * Only B12 and folate can make cells megaloblastic (hypersegmented). Microcytic or macrocytic all have to be chronic. If you have an acute situation. The patient has never had symptoms. The low threshold for antibiotics is because these patients are immunocompromised due to function asplenia. reticulocyte count. * Hematologically. dehydration. But. * Give sickle cell patients antibiotics without obvious signs of infection if they simply have a fever or leukocytosis. You note no lower extremity ulcers (a complication of sickle cell). Peripheral is the most common. lung). 47yo man comes to the Emergency Department with a history of sickle cell and complains of terrible pain in the chest. and infection predispose sickle cell patients to sickling.79 - . rare Diphyllobothrium latum fish tapeworm). So for exchange transfusion you get rid of half of their (homozygote) blood and replace it with normal blood. * 21yo patient asks about testing because his father gets treated for sickle cell. A few hours later he is worse with blurry vision because the sickle cells have reached his eyes. * Hydroxyurea is used for prevention of sickle cell crisis. How should you manage this patient? * Most accurate or specific test is electrophoresis for sickle cell. * Hyperuricemia can only occur in cells that have the purines and pyrimidines of nuclei. * Increased bilirubin can be seen in hemolysis. In reality. O2 Sat 100% on room air. * Treat the above 47yo patient with oxygen. If you see hypersegmented polys. you have to order both the folate and B12 levels. myeloma. But you do not have to have one before the other. you can get any neurologic issue that you see on a neuro exam. So B12 deficiency can occur without neurologic problems. * All forms of hemolysis have normal MCV (80 to 100). * Methylmalonic acid used with equivocal B12 level. CNS disturbances. like leukotriene antagonists for asthma prevention. The smear can tell the difference between sickle cell trait (heterozygous) and disease (homozygous). RR of 12. it goes up in B12 deficiency. peripheral neuropathy. decreased vibratory sensation. not history of osteomyelitis (most common staph aureus. You cannot get thalassemia or iron deficiency in the acute setting. He is asking for narcotics to treat his. * Any patient with neutrophil count < 500 and a fever should get antibiotics (neutropenic fever). acidosis. DO NOT DISTRIBUTE . fluids. Schilling test is only done when you know you have B12 deficiency and you want to know the cause (bacterial overgrowth blind loop syndrome. not hemolysis because no nuclei. Sign nonspecific tissue damage. paroxysmal nocturnal hemoglobinuria (PNH). and thighs. You tell him you think he is not in pain. autoimmune. leukemia. no aseptic necrosis of the femoral head. and drugs can make cells macrocytic (large cells) but not megaloblastic. brain. * Say you gave the 47yo patient oxygen. but not the neuro problem. which basically turns them into a heterozygote. rhabdomyolysis sometime. sickled cells occur in the disease. salmonella only happens in sickle cell). then you know it is due to folate or B12. * Reticulocyte counts will be high. and bilirubin do not tell you if the patient has sickle cell.Study Notes – Internal Medicine James Lamberg 28Jul2010 megaloblastic cells. Hemolysis is the only one that can be acute. Alcohol. blood. Hemolysis * Causes of hemolysis include sickle cell disease. subacute combined degeneration of the cord which accounts for the vibratory sensation problems and looks like tabes dorsalis. back. lymphoma. Neurologic problems are memory loss. * Treatment of folate deficiency is…wait for it…folate. * Sickle cell in 1 of 400 African Americans and 8% have the trait. These patients can die from pneumococcal or hemophilus sepsis very quickly. there is no difference between folate deficiency and B12 deficiency. * B12 deficiency has neurologic problems. We also know that patients can sickle without any of those things. Patients with sickle cell trait will have a normal smear. good sensitivity but poor specificity. Some will have a low haptoglobin if the cells are destroyed in the vasculature because haptoglobin takes freely released hemoglobin to the spleen for recycling. tissue destruction (muscle. folate deficiency does not.
It is an old test. Leukemia * Forms: Acute myelogenous leukemia (AML). The problem is when the spherocyte meets the spleen and cannot get through hemolysis occurs. found on routine screening. carbamazepine. isosthenuria. kidney infections. * What is the normal drop in hematocrit with a sickle cell crisis? Answer is none. * Homozygous sickle cell patients can have sickle cells even without crisis. Spherocytes are the opposite of a target cell. fava beans. In asymptomatic patient. it does not happen right away. nutritional DO NOT DISTRIBUTE . cephalosporins. this is an acute drop in cells that is not blood loss. primiquin use. The antibodies attach to the RBC and take out little bites. so that is the treatment. measuring a G6PD level will show a normal level. it just removes the cause of hemolysis. avoid certain drugs. * Treatment is to remove sources of oxidant stress. lymphoma. * Acute forms are immature cells. kills you slower (6-12 years even without therapy). * The problem is not that you have spherocytes. low or dysfunctional white cells gives high fever and infection. * Spherocytosis is diagnosed with an osmotic fragility test. sulfa drugs. do splenectomy. it binds up the oxygen and causes localized hypoxia to provoke sickling. benzene use. acute lymphocytic leukemia (ALL). We know acute leukemia can be caused by chloramphenicol. * Paroxysmal nocturnal hemoglobinuria (PNH) presents with just that complaint. like SLE. thrombocytopenia gives bleeding. * G6PD deficiency is the only hemolysis cause that has an enlarged spleen because it is chronic. * Coombs test differentiates autoimmune hemolysis from other forms of hemolysis. * Acutely. If there is a drop in hematocrit with sickle cell crisis think about aplastic crisis from parvovirus B19 or folic acid deficiency (no storage form). * Oxidized iron in a RBC (precipitated oxidized hemoglobin) is Heinz bodies. where metabisulfite is added to blood. * There is no known cause for chronic leukemias. * Causes of pancytopenia include cirrhosis and portal hypertension causing hypersplenism as the spleen can sequester all three cell lines. Thrombosis of large vessels (DVTs. Chronic forms are more mature cells. chloramphenicol). bone marrow depressing drugs (most common alcohol. Answer is renal disturbance such as hematuria. If it keeps recurring. Splenomegaly takes time. and chronic lymphocytic leukemia (CLL). kills you quick (as short as 6-12 weeks). which has a compact hemoglobin and a big floppy membrane. * Sodium metabisulfite test is a screening test for sickle trait that is sometimes used. they carry oxygen and CO2 just fine. This cell travels to the spleen and the spleen takes little bites of the iron. think of the drugs people are generally allergic to. * Drugs that cause autoimmune hemolysis penicillins. * Osmotic fragility test swells the cells a little bit causing lysis. * Treatment of bad autoimmune problems is steroids. leaving bite cells. a CBC and peripheral smear will not be helpful. certain drugs. rifampin. radiation. Autoimmune is the only one that is Coombs test positive. Thus. the problem is not the cell it is the spleen. etc. Anemia gives malaise. eventually converting into a sphere. Half the time it is idiopathic. dapsone use. * Presentation for AML and ALL is based on the severity. The same drugs cause allergic interstitial nephritis. portal vein thrombosis) can occur but we do not know why.Study Notes – Internal Medicine James Lamberg 28Jul2010 Test of choice here is electrophoresis. sulfa drug use. so you can lose 20-30% of your hematocrit via reticulocytes over the next few days. Autoimmune hemolysis has spherocytes as well on peripheral smear. radiation. * PNH responds to steroids for unknown reasons. methotrexate. The malarial also does not recognize the cell as well because it is lacking certain receptors. Wait for a couple of months then do a G6PD level.80 - . Splenectomy does not remove the spherocytes. pancytopenia. don’t eat fava beans. * Patients with sickle cell disease are protected from malaria because when the falciparum enters the cell it acts as an oxidative stress so the cell commits suicide and hemolyzes. any primary or metastatic cancer. Less common worries would be getting sickle cell while climbing Mount Everest. Most common oxidative stress is infection. Like all other forms of hemolysis. Most people do not get up to urinate at night. So the smear can tell you if someone has the disease but cannot help you differentiate normal from crisis. but that could happen. Patient asks what that means for him. * G6PD deficiency associated with Mediterranean descent. They can be used to tell you that you have G6PD deficiency. * Parvovirus freezes the bone marrow. Testing shows sickle cell trait. autoimmune (SLE). Diagnosis cannot be made on history. This is because the most deficient cells are destroyed leaving the normal cells behind. so they see the hemoglobinuria in the morning. aplastic anemia. chronic myelogenous leukemia (CML). * Autoimmune hemolysis should be considered as the cause when you have signs of hemolysis and a history of autoimmune disease. Also some genetic counseling. portal hypertension. Mnemonic: It is like becoming allergic to your own blood.
marrow-invading infections (TB. * Side Note: Treatment of multiple myeloma is melphalan and prednisone. Average survival for this guy is 10-12 years. normal in 1/3. virus). * Patient at clinic for routine exam and found to have high white count. and they have the same initial therapy. low in 1/3. then look for Philadelphia chromosome. not at state 1 which is lymph nodes. Then you do another round and remove 99. but hematologist/oncologists call this a sustained remission. * For ALL and AML. Philadelphia chromosome codes for tyrosine kinase. anemia. pro-myelocytic. So these cells look normal but have abnormal function. * CLL Stages: 3 – anemia. Marrow transplant is an option. * Patient who is 50-60yo with CLL and advanced stage disease (hypersplenism. and prednisone. There is no equivalent of Gleevec for CLL so we’re stuck with carpet bombing via chemotherapy. CML cell on smear does not look different from normal neutrophil. * CLL Stages: 0 – increased WBC. This is a 10-12yr survival. * An enlarged spleen is most characteristic of CML. CML differential will be 90% neutrophils/polys. no therapy. a silver bullet. they begin to divide and 6 months later you have leukemia again at the brink of death. This is no good because these patients die. * Wait. Aplastic Anemia * CBC has WBC.9% of what was left (consolidation). Japanese women live the longest to age 84. * CML can convert to ALL in about 20-25% of patients (“blast off”). Average age of man in United States is 76. eosinophils. lymphocytes. so this drug specifically inhibits the tyrosine kinase.000 lymphocytes particularly because you need to get a bone marrow biopsy for that. * Chronic leukemias always have high white counts. then you are more confident it is CML which is associated with Philadelphia chromosome. Interferon is another option as it makes the Philadelphia chromosome negative. Retin-A for acne is cis retinoic acid. What is the diagnosis? CLL. vincristine. which causes DIC.000 white cells. Now what? Answer is do nothing. * Treatment for CLL is chlorambucil and prednisone. This leukemia is a little different because you can give CNS prophylactic therapy with intrathecal methotrexate. RBC. do a bone marrow transplant.9% of cells. * With recurrence after chemotherapy agents. Medical therapy is Gleevec (imatinib mesylate). The others are indistinguishable with initial tests. If all the cells were not removed. “a little tired. Fludarabine if that does not work. * Treatment for AML is daunorubicin and Ara-C (cytosine arabinoside). The ultimate goal of chemotherapy is to remove so many cells that your body can eliminate what is left. * CML M3 is treated with all-trans retinoic acid (vitamin A derivative). do a round of chemotherapy to remove 99.9% of what was left (maintenance). You wouldn’t use fluconazole to try to kill bacteria. When you see the high neutrophils. You wouldn’t use acyclovir to try to kill fungi. What is the next step? Answer is differential. This is how you pick up CML and CLL. * You made leukemic cells today. Your immune system eliminated them. myeloperoxidase. The differential shows 93% lymphocytes. We would call this a cure. The same goes for leukemia drugs. Lymphocytes have T-cells and DO NOT DISTRIBUTE . * Exception is M3. fungus. This is a 1-2yr survival. * M3 also has Auer rods.Study Notes – Internal Medicine James Lamberg 28Jul2010 deficiency (B12 and folate). 4 – low platelets.” * Patient found to have 62. How do you distinguish CML from CLL? * CLL cell on smear does not look different from normal lymphocyte. These patients are generally too old for bone marrow transplants. like stepping on a jelly donut. One round of daunorubicin and Ara-C takes out 99. 1 – lymph nodes. Acute leukemias are high in 1/3. They all present the same so no real need to know them unless you are an oncologist. thrombocytopenia) should be treated with chlorambucil or fludarabine. what about the 73yo man with leukemia? You are going to just leave him with no therapy? He is at stage 0 with just a high white count.9% of leukemia cells in the body (remission induction). Then you stop so the patient doesn’t die. cALLa seen in ALL (common ALL antigen). * The difference between all those causes and acute leukemia is blasts. but there were so many cells to start with that three rounds are needed. * 73yo man comes to your office for advice on diarrhea prophylaxis prior to a trip to Mexico. Yes you may see some smudge cells with CLL as you are putting down the cover slip it smudges the fragile cells. * CLL differential will be 90-95% lymphocytes.000.81 - . * You didn’t want to get a Philadelphia chromosome on the patient with 62. Results from routine tests from a previous visit show a WBC of 75. Marrow transplant is an option. * You wouldn’t use metronidazole to try to kill viruses. platelets. * High white count with nearly all neutrophils on differential. This seems like a huge change. * Side Note: 25% of the population feels “chronic fatigue” at any given time. * Treatment for CML is bone marrow transplant if donor. Then a third round to remove 99. WBC has neutrophils. This is why we transplant immediately if a donor exists. * Treatment for ALL is daunorubicin. * The 7-8 different types of acute leukemia (M0-M7) cannot be distinguished from history and initial tests.
it’s a trick you want to kill me. rolls over in bed and gets broken bone. You do an electrophoresis that shows a monoclonal spike. * Immunoglobulins made against a single antigen (monoclonal). alcohol. Plasma cells also making Bence-Jones protein (immunoglobulin parts that end up in urine). no humerus fracture from leaning against something. What is the best thing to do next? Answer is staging because treatment is based on stage. platelets? What is this. Plasma cells are 5%. Give this to the patient. If chest CT negative. * How do you determine if local? You could start with CXR. give medications (ATG. such as in marrow. T-cell subtypes range from CD1 to CD134 thus far. cyclosporine). autoimmune (for unknown reasons). cells are like “yo buddy we’re the eosinophils you’ve always been with” and T-killer cells is like “uhh. * Treatment is melphalan and prednisone. * Stages have A and B. whoa. * CXR negative. night sweats. chest CT. Excisional biopsy comes back positive for Hodgkin lymphoma.” The only person who can see this magic antigen is the body. then could do chest CT.Study Notes – Internal Medicine James Lamberg 28Jul2010 B-cells. no pathologic fractures. then abdominal and pelvic CT.g. Needle biopsy is not good enough. * Stage III: Both sides of the diaphragm. weight loss. CLL and lymphoma are very similar. Patient says he does not have bone pain. * If your T-cells were injected into a horse. with plasma cells delusional creating antigens against some antigen. Stage II: Two groups of lymph nodes. There is some leeway here. * Early stage (I to IIa) is radiation and late stage (IIb to IV) is chemotherapy. * Hodgkin disease 80-90% of the time presents in stage I or II. uric acid (hyperuricemia). where patient is not immunosuppressed as much. * So one day the T-killer cell wakes up and says. Calcium level is normal. If it showed mediastinal and hilar lymph nodes for this 32yo with a neck mass. T-cells knocked out. DO NOT DISTRIBUTE . It is difficult to transplant patients with myeloma because this occurs in older individuals and the transplant itself can kill the patient. they are abnormal lymphocytes that look relatively normal on smear. who are you guys? B-cells. If no donor. laparotomy (e. T-killer. * Treatment for autoimmune aplastic anemia is bone marrow transplant if you are young and have a donor. same side of diaphragm. * Most of the time with aplastic anemia it is autoimmune. how did you get into my marrow? T-killer cell develops homicidal ideation. If all of these are negative. I’m here to kill you” but body says “don’t bother me. * Most common complaint is unexplained bone pain. * Testing for localization: CXR. alcohol. * A needle biopsy smear will look normal. This is anti-thymocyte globulin (ATG). reset the bone marrow. but this is just to reduce the number of cells. * Staging is important. No Bence-Jones protein in urine. * Non-Hodgkin disease 80-90% of the time presents in stage III or IV. radiation use is to stop the offending agent. * Man comes to you because his total protein was found to be elevated on routine visit. specifically suppresses the T-cells. Think myeloma with non-traumatic bone pain in old person. drug. no you’re not. osteoclast activating factor (OAF) which goes to bones and seeps calcium into serum. Treatment is stem cell transplant. Lymphoma * 32yo woman presents with neck mass. the horse would make antibodies against them. well I’m going to kill you first!” The T cells start to kill the rest of the marrow. Older people do not recover well when made pancytopenic and neutropenic with chemotherapy prior to marrow transplantation. Say abdominal and pelvic CT showed lymph nodes consistent with lymphoma in the 32yo with neck mass? Answer is chemotherapy because she is at stage IIIb. “Hey buddy. 1% of these patients go on to myeloma but we cannot determine who does. I’m fighting another antigen. Normal uric acid level. No anemia or renal dysfunction. What do you do next? * Answer is no treatment. in spleen not seen on CT). benzene. abdominal and pelvic CT. bone marrow aspiration (lymphangiogram was old test). used in kidney transplantation. What would you do next to determine the diagnosis? Answer is excisional biopsy. sweats. * Myeloma is > 10% plasma cells for diagnosis. B is symptoms of fever. * Older patient who coughs and causes ribs to break. no salt and pepper head.82 - . she is going to die. * Stage I: One group of lymph nodes. which is aplastic anemia. This disease is called monoclonal gammopathy of undetermined significance (MGUS). So she would get chemotherapy. weight loss. You need to see architecture. Stage IV: Diffuse disease. fever. * What drugs would you use to suppress T-cell function? Cyclosporine. It is so busy creating antigens and fighting this unknown/nonexistent thing that real infections run rampage. * Aplastic anemia can be from drugs. If you radiate her neck and she has disease in her pelvis. a defect in the T-cell. then you can radiate a local lymphoma. she is at stage IIb. bone marrow comes back. Myeloma * Plasma cells are making IgG and IgA that are detectable on serum protein electrophoresis. Pneumococcus shows up in the body. * Treatment if chloramphenicol. This implies a worse prognosis.
It is not hemophilia because she is a woman. Bleeding time is a test of platelet function. Then you time the bleeding. This is the ristocetin test (artificial endothelial surface). where it is made and stored. Fibrin is broken to D-dimers (fibrin parts) by plasmin. leading to good clotting. * Treatment of Hodgkin lymphoma is ABVD/MOPP. * How do you do bleeding time? You put on a BP cuff to occlude the veins of the arm. IX) are clean because they are no longer pooled blood products. * 26yo with platelet-type bleeding. * Vitamin K deficiency: prolonged PT. Cryoprecipitate is pooled blood products and can transmit disease. platelet count low. Her prothrombin time is normal at 11s. increased PT. normal platelets. PT is normal. you could look at the empty beer bottles (D-dimer) or the bottle caps that were split off (fibrin split products). What is the most likely diagnosis? This is platelet-type bleeding with a normal platelet count. Fibrin split products gets split off from fibrinogen to activate it to fibrin. Then get a von Willebrand factor level. * After the initial clot is formed via vWF with platelets and endothelium. fever. so do not do a bleeding time if the platelet count is low (< 50. * DIC has low platelets.000. with factor-type and platelet-type bleeding. So do bleeding time when you see platelet type bleeding with a normal platelet count. What is the treatment? Steroids. * Treatment of von Willebrand disease is desmopressin (DDAVP). von Willebrand disease. * Von Willebrand disease: normal PT. fibrin come in and cross-links the clot. * Desmopressin releases sub-endothelial stores of vWF. What is the next test for diagnosis? Answer is antiplatelet antibody test. MOPP. platelet count of 217. prolonged/normla PTT. normal platelets. gums. 1% will develop aplastic anemia.Study Notes – Internal Medicine James Lamberg 28Jul2010 * Treatment of non-Hodgkin lymphoma is CHOP. * First thing to do with a bleeding question is determine the nature of the bleeding before you look at the labs. Excision biopsy shows Reed-Sternberg cells. * It is not vitamin K deficiency because PT is normal. * Radiation of local disease results in a cure 90% of the time. thus it is not used much. What is the next step in management with the assumption of von Willebrand? Answer is bleeding time (prolonged). normal platelets. Vincristine and vinblastine causes peripheral neuropathy. What would you do next in the management of this patient? Stage is IIIb so do chemotherapy with ABVD/MOPP. Is this factor related bleeding (deep like hemarthrosis in joint. platelet-type bleeding. but enough so the artery is open. If you have platelets and ristocetin with vWF present they will stick. so increased in ITP. * They tell you the spleen is normal to rule-out splenic sequestration. Factor VIII and vWF sit in the endothelial lining. coli and recombinant technology. Cyclophosphamide causes hemorrhagic cystitis. * Megakaryocytes are precursors to platelets. * In order for platelet and endothelium to stick to each other they need vWF. so in the 26yo patient so most likely von Willebrand since it is the most common hereditary coagulopathy. If DDAVP does not work. Adriamycin gives cardiac toxicity. * If you wanted to know how many beers someone drank. then you might give cryoprecipitate. Then you take a razor blade and cut the patient. PTT normal. * 32yo woman with a neck mass. * TTP is associated with renal failure and hemolysis. you need an artificial endothelial surface. PTT is prolonged at 52s. the platelets do not stick to ristocetin. Pelvic CT scan is positive for lymph nodes consistent with lymphoma. * Factor replacements (VIII. prolonged PTT. Factor XIII helps preserve the clot.83 - . Cisplatin causes nephrotoxicity and ototoxicity. skin. The spleen is not enlarged on exam. * Most common side effect of chemotherapy (CHOP. Tissue plasminogen activating factor (tPA) so that the plasminogen turns into plasmin and then the plasmin chops up the fibrin linked clot. This is idiopathic thrombocytopenic purpura (ITP). weight loss. mucosa. increased PTT. Bleeding Disorders * 26yo woman presents with epistaxis and petechiae. * Glanzmann thrombasthenia and Bernard-Soulier syndrome are rare. Why don’t we just chemo everyone? Side effects. 1% a year develop AML. DO NOT DISTRIBUTE . but you need a bone marrow biopsy to see these. factor-type bleeding. night sweats. Testicles are more vulnerable to this effect. If that doesn’t work. To see if there is functional vWF. so it is not unusual to see prolonged PTT in von Willebrand disease. This rapidly brings up the vWF level. ABCD) is sterility in 95% of patients. normal PTT. * Say you have platelet-type bleeding with normal platelet count. * Factor VIII antigen (vWF) travels bound to the factor VIII coagulant portion (hemophilia).000) because bleeding time will always be abnormal. factor-type bleeding. give factor VIII replacements because it comes with some von Willebrand factor (vWF). If vWF is not there. vagina)? * Hemophilia: normal PT. * Busulfan and bleomycin cause pulmonary fibrosis. hematoma in muscle) or platelet bleeding (superficial like epistaxis. They are made with E. Hepatitis B vaccine is made this way too.
and PIPs are red and swollen on both hands. usually presents in young adults. Not CXR. and other acute phase reactants like C-reactive protein (CRP). If you give vitamin K and the patient gets better it was vitamin K deficiency. What do you do next? * Hemophilia presents as a child that slides into base playing baseball and gets a hemarthrosis. platelet count is low. * Ratio is about 3:1 women to men for RA. Thus. DIPs are almost never involved. ferritin normal or high because ferritin can act as an acute phase reactant). high platelet count. On exam the wrists. can get fibrosing changes causing restrictive disease. liver function. PTT is normal. if labs do not change it is liver disease. give FFP. normal platelets. The surgeon sends the patient to you because the PTT is prolonged. Test for autoimmune hemolysis is antiRBC antibody (Coombs) versus antiplatelet antibodies for ITP. She also has pain in her wrists. this is the quickest way to raise the platelet count. If patient recurs then do splenectomy. She denies back stiffness or back pain. not inflammation. epidural hemorrhage. Glucose could be up as a complication of steroids. * Extra-articular manifestations of RA include splenomegaly and neutropenia (triad is Felty syndrome). Another manifestation is pulmonary nodules (Caplan syndrome). Classic MCP and PIP involvement and the joint involvement is symmetric. but usually not necessary. high CRP. * Rubor (red). loss of energy have corresponding inflammatory laboratory results such as anemia of chronic disease. * Treatment of lupus anticoagulant is to replace factors. MCPs. Rheumatoid Arthritis (RA) * 26yo woman with no prior medical history presents with a three week history of joint swelling and stiffness. DO NOT DISTRIBUTE . * Liver disease has very high PT. meaning RA with positive rheumatoid factor. DVTs.” * Macrophages bring the platelets that have antiplatelet antibodies and drag them to the spleen for processing. PT is normal. normal platelets. do an arthrocentesis. As a side point. PT is normal. * If a joint is swollen and/or fluid filled compared with other joints. radioactive material. it has a half-life and will decay. not x-rays of lumbosacral spine. although it can be seen in other disease. Arthralgias are joint aches. they only help confirm diagnosis. glucose level. this is 20 joints involved so polyarticular. * 26yo woman with platelet-type bleeding. * Constitutional symptoms are fever. dolor (pain) for joints inflammation. myasthenia crisis. melena. weight loss. calor (hot). History of recurrent abortions. high PTT. Normal electrolytes. a PE before. * Labs looking for anemia of chronic disease (MCV low normal. There is a circulating antibody (Guillain-Barré. subdural hematoma. an autoimmune disease. So this patient has ITP and is bleeding into her brain and bowel. increased platelet count. The distal interphalangeal (DIP) joints are not involved. TIBC low. * Lupus anticoagulant: Elevated PTT. * At least 70% of patients are have seropositive RA. normal PT. not CT scan of head. Goodpasteur. loss of appetite. Or. * Diagnosis is not made by a single serologic test being positive. not ECG. * This is very much like autoimmune hemolysis. * 62yo man has a prostate mass and is going to get a biopsy. loss of joint space and inflammation. Steroids for both.84 - . ITP) why not get rid of it? Just not necessary in most cases. Splenectomy is the steroids fail and the patient recurs. PEs. * In RA.Study Notes – Internal Medicine James Lamberg 28Jul2010 * Treatment of ITP is steroids. * Plasmapheresis sounds like a good idea. Thus the platelets are not processed. What is the next step in management? IV Ig or RhoGAM. Asher Kornbluth. Pyloric stenosis because you’ll see it again [the food]. She points to all her proximal interphalangeal (PIP) joints as well as the metacarpal phalangeal (MCP) joints. * Morning stiffness is a classic disease marker for rheumatoid arthritis. C1-C2 joint is the only area of the spine that can be involved in RA. * What is the most likely diagnosis in the 26yo woman? Rheumatoid arthritis. high sedimentation rate (Sed rate). Increased reticulocytes are like increased megakaryocytes. * Serologic tests include rheumatoid factor (IgM antibody against IgG). * “Memorized learning or non-understood learning is one of two things. night sweats. Psoriatic arthritis is similar to RA but psoriatic arthritis affects DIPs. kidney function. The patient has no bleeding history and has had prior surgeries without event. * Fresh frozen plasma (FFP) has no platelets. * What imaging tests would be abnormal in this patient? Hand joint x-rays showing erosions in the joint space. like a monoarticular arthritis with a single red hot knee or do they have polyarticular arthritis affecting a few joints (oligoarticular arthritis) or more diffuse with or without symmetry. high ESR. platelet count is normal. -------------------------------------------------------------------------------------------------------------------------------------------Kaplan Videos (2001) – Rheumatology with Dr. MD -------------------------------------------------------------------------------------------------------------------------------------------* Pay attention to the number of joints involve. He did have a DVT three years ago and last year. Giving IV Ig stuffs up all the Fc receptors on the macrophage. She has fatigue and low grade fever (think generalized inflammatory condition). subarachnoid hemorrhage as well. Fe low. * The only hypercoagulable state that has an elevation in bleeding labs (PTT increased) is lupus anticoagulant. She has stiffness for two hours every morning since these symptoms started and the symptoms improve as the day progresses.
Study Notes – Internal Medicine
* Arthrocentesis: non-inflammatory (osteoarthritis/DJD) has WBC < 2,000/mL, inflammatory (RA) has WBC from 5,000 to 50,000/mL, septic joint has WBC > 75,000/mL. * Say patient has RA with symmetry except for a knee that is 3x larger than the other knee. Arthrocentesis shows WBC 100,000/mL, so that joint is also infected. * Treatment for mild RA is aspirin or NSAIDs, both shown to be as effective. * Major complication of aspirin (ASA) and NSAIDs is upper GI ulcer and bleed. This is still a cause of death in the elderly. Aspirin toxicity at high dose can cause tinnitus and high anion-gap metabolic acidosis that is also associated with a respiratory alkalosis (increased respiratory drive). Interstitial nephritis is an uncommon complication of aspirin. NSAID complications also include renal insufficiency, especially in the elderly who can be dry. NSAIDs can affect CNS, confusion and delirium in high doses. * Acetaminophen is not an anti-inflammatory, thus it is not used in inflammatory disease like RA. Side-effects of acetaminophen (APAP, paracetamol) include liver toxicity and does not cause upper GI ulcers. * Arachidonic acid is metabolized to phospholipase into 2 pathways, cyclooxygenase (COX) and lipoxygenase. Products of COX are prostaglandins and prostacyclin. Products of lipoxygenase are leukotrienes, which are proinflammatory. Prostaglandins mediate inflammation and pain. Prostaglandins are also cytoprotection mediators in the stomach and are helpful for renal blood flow. * COX comes in COX-1 and COX-2. Cytoprotection in stomach is part of COX-1. Renal vasoconstriction is part of COX-1 blocking. Inflammation and pain are part of COX-2. Thus blocking only COX-2 would relieve the pain and inflammation while preventing COX-1 renal vasodilation and maintaining COX-1 cytoprotection. * Celecoxib is a COX-2 selective inhibitor. Rofecoxib was pulled from the U.S. market in 2004. * Treatment for RA should not include long-term steroids because of complications. Steroids are used in the shortterm for a patient that is not relieved with aspirin or NSAIDs. * Disease modifying anti-rheumatic drugs (DMARDs) include gold, penicillamine, azathioprine, and methotrexate. The most useful drug is methotrexate for long-term maintenance of RA. * Methotrexate (MTX) side-effects include liver fibrosis, cirrhosis particularly with cumulative high doses, pulmonary hypersensitivity reaction, bone marrow suppression. * RA patient presents with fever, pleuritic chest pain, infiltrate, and is on DMARD therapy. Answer is stop the methotrexate and give steroids for pulmonary hypersensitivity reaction. * What lab test should you following in a RA patient on long-term MTX? Answer is LFTs and CBC. * Any patient on MTX should also be on folate to help reduce the risk of bone marrow suppression. * Steroid toxicity is common so might as well put steroids on the problem list if a patient is taking them long term. * Steroid toxicity includes cataracts, glaucoma, psychosis, personality disturbances (anxiety, depression, moodlability), uncommon CNS infections like Listeria monocytogenes meningitis (not seen in immunocompetent), candidal thrush, moon facies (big, round), osteopenia and osteoporosis even at a young age, aseptic necrosis (avascular necrosis, osteonecrosis), increased risk of GI bleed. * Osteoporosis with steroids is dependent on dose and duration of steroid use. * Lab test abnormalities with steroids include metabolic alkalosis and hyperglycemia. * Rheumatoid arthritis patient presents with a swollen painful calf. There is no palpable cord and the patient has no risk factors for DVT. This is ruptured Baker cyst in the popliteal space. No need to do diagnostic tests here. * Patient presents after a motor vehicle accident. They have a history of rheumatoid arthritis. What should you be careful of during intubation? Do not hyperextend the neck due to chance of atlantoaxial joint (C1-C2) subluxation. Systemic Lupus Erythematosus (SLE) * 35yo woman is brought for the evaluation of confusion for a day. Her friends and family inform you that she did not know how to get home from work and lately she has not been herself. You find that the patient has elevated blood pressure, decreased air entry at the right lung base with dullness to percussion (pleural effusion), and symmetrical joint swelling of the wrists and MCPs. Chemistry profile shows an elevated creatinine to 2.4 and there is protein in the urine on urinalysis. What blood test might you use to confirm your suspicion? * Anti-mitochondrial antibodies seen in primary biliary cirrhosis (PBC). * Anti-histone antibodies seen in drug-induced lupus. * Anti-double stranded DNA antibodies seen in lupus, particularly specific in active lupus with renal involvement. * Anti-centromere antibodies seen in scleroderma (CREST). * Anti-smooth muscle antibodies seen in autoimmune hepatitis. * Anti-nuclear antibodies (ANA) is very sensitive in lupus, so it will be positive in most cases of SLE but there are many false-positives. If ANA is negative though, it helps rule out lupus. * You rarely see a patient with lupus that has joint involvement as their chief complaint. * Ratio is about 10:1 women to men for lupus.
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Study Notes – Internal Medicine
* Symptoms of lupus include CNS (lupus cerebritis causing change in mental status, change in personality, depression, psychosis, seizures), alopecia, malar “butterfly” purple rash, discoid lupus (purplish disc-shaped discoloration usually after sun exposure), aphthous ulcers, pleural effusions (lupus serositis), pericardial effusion, sterile vegetation on heart valves (less common, Libman-Sacks endocarditis), renal disease (glomerulonephritis which is hallmarked by RBC casts in urine and proteinuria in nephrotic range), recurrent second trimester abortions due to hypercoagulability from anti-phospholipid antibody (lupus anticoagulant) causing placental vessel thrombosis, joints typically symmetric with arthralgias more than arthritis. * Labs abnormalities for lupus include mild leukopenia, anemia of chronic disease, autoimmune hemolytic anemia, autoimmune thrombocytopenia (decreased platelets, ITP), renal insufficiency (increased creatinine), RBC casts and protein in urine. * Serology for lupus includes positive ANA (peripheral rim pattern), anti-DS DNA, low complement level (CH50) particularly with active lupus nephritis, less likely is anti-Ro (SSA) and anti-LA (SSB) antibodies. * Anti-Ro antibody is associated with neonatal lupus (mother has anti-Ro), babies get complete heart block. * Drug induced lupus causes include hydralazine, procainamide, isoniazid, alpha methyl-dopa. * These patients have prominent serositis, so pleural effusions and pericardial effusions. * Symptoms include arthralgias, fever, fatigue, no CNS involvement, no kidney involvement. * Patient presents with pleural effusion, fever, joint soreness, malar rash, increased creatinine, personality changes. They are taking hydralazine for hypertension. What antibody should you check? Answer is anti-DS DNA because this is true lupus and not drug-induced. Drug-induced would not have CNS or kidney involvement. * Test for drug-induced lupus is anti-histone antibodies. These patients can get false positive VDRLs, they will not have a positive FTA (fluorescent treponemal antibody). * Treatment of SLE is complicated and usually done by the rheumatologist. Know basic drugs though. * Treatment of SLE is NSAIDs for arthralgias and serositis. Steroids used for CNS involvement, kidney involvement, and autoimmune hematologic problems. With nephritis, if steroids are not enough add cytotoxic drugs like cyclophosphamide or azathioprine. * Treatment for SLE with second trimester abortions includes aspirin or low molecular weight heparin to preserve the pregnancy and prevent a thrombotic event. * Treatment for SLE includes liberal use of sunscreens. Scleroderma * 36yo woman comes to you because of skin tightness and painful fingertips with exposure to cold. These symptoms have occurred for over one year. Exam notes tight skin on the face with a shiny appearance. BP is 165/100. Laboratory tests reveal a macrocytic anemia and elevated creatinine. What is the diagnosis? Scleroderma. * Scleroderma is more common in women. * Painful fingertips with exposure to cold is Raynaud phenomenon, which is not unique to scleroderma. Color changes can occur (white, blue, red). Sensitivity can be so exquisite the patient cannot walk into a room that has air conditioning running without their hands becoming painful. Patients may wear gloves in the summer time or be unable to hold a cold iced drink. * Sclerodactyly is skin tightness of the fingers that is so tight it causes bone resorption. * Progressive systemic sclerosis (PSS) is a term to denote scleroderma patients with the most severe disease. Renal involvement is the organ to worry about here and can lead to death, not seen in CREST syndrome. * CREST syndrome is the milder form of scleroderma. * CREST: calcinosis (calcium deposits), Raynaud phenomenon, esophageal hypomotility (severe reflux), sclerodactyly, telangiectases (usually on face). * Esophageal smooth muscle and LES replaced with collagen, leading to worse GERD you may ever see. * Renal involvement in PSS is exacerbated by elevated blood pressure. This is because the renal arteries are replaced by collagen and cannot dilate appropriately, so low renal blood flow due to sclerosis of the renal vessels. The kidneys behave as if they are pre-renal (vasoconstricted), triggering the RAAS pathway. * Treatment of choice for scleroderma with hypertension is ACE-I (lisinopril, captopril, ramipril) to block RAAS. If the patient cannot tolerate ACE-I (e.g. cough), give angiotensin II receptor blocker (ARB) like losartan. * ACE-I cough is an allergic phenomenon related to bradykinin alterations. * 36yo woman with scleroderma, has painful fingers, horrible GERD, hypertension, calcinosis. What is the most important symptom to treat? Answer is treat hypertension aggressively; this is critical to prevent renal crisis. * Treatment should not involve steroids, they are not beneficial in scleroderma and have major side-effects. * Treatment for scleroderma is ACE-I primarily for hypotension. * Treatment for scleroderma can includes penicillamine (some skin manifestations) and calcium channel blockers like nifedipine or nitrates (Raynaud phenomenon).
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Study Notes – Internal Medicine
Sjögren Syndrome * 42yo woman presents with some peculiar symptoms that she has had over the past year or so. She informs you that she feels there is constantly something in her eyes like dust or sand. She says dry and solid foods are painful to swallow. You are perplexed by her complaints but decide to examine her and find that she has bilateral parotid enlargement but otherwise an unremarkable examination. An ANA test is positive. What specific ANAs do you expect to be positive in this patient? * Triad of dry eyes, dry mouth, and parotid gland enlargement is Sjögren syndrome, an autoimmune disease. * Sjögren syndrome sometimes found by itself, often found in association with other autoimmune diseases such as lupus, rheumatoid arthritis, and scleroderma. A combination of diseases is considered a mixed connective tissue disease (MCTD). These patients tend to have an antibody known as anti-RNP (ribonucleoprotein). * Diagnosis is suspected based on clinical presentation, reinforced with anti-RNP if associated with MCTD. * Schirmer test measures moisture in the eyes (decreased tears). Biopsy of salivary glands shows lymphocytic infiltration. ANA can be positive, also anti-Ro, and anti-LA antibodies. * Treatment is symptomatic with artificial tears and sucking candies, not usually a majorly disabling disease. Ankylosing Spondylitis * 27yo man presents with complaints of severe lower back pain and stiffness that have been bothering him for the past five years. He informs you that the stiffness is more apparent in the morning when he awakes, lasting sometimes for more than two hours. The only thing improving these problems is exercise. On exam he has a 2/4 diastolic murmur over the second right intercostal space and decreased range of motion of the lumbar spine. What is the most likely diagnosis? Ankylosis spondylitis. * Ankylosis spondylitis also associated with sacroiliitis, fusion of the SI joint. The first x-ray finding may be this fusion, suspected when there is this presentation and pain in the pelvic girdle area. This is associated with IBD; the two conditions (IBD and ankylosing spondylitis) can follow independent courses. * Not many pains improve with exercise, this is one of them. RA spares the back, so even though there is morning stiffness you can basically rule out RA. * Seronegative arthropathies (spondyloarthropathies) are more common in men than women. These often have prominent extra-articular manifestations. Genetic marker HLA-B27 positive in most of these. * Aortic insufficiency often seen in ankylosing spondylitis, unknown cause. * There is typically a lumbar lordosis and thoracic kyphosis in normal patients. Ankylosing spondylitis patients lose this curvature giving a straight spine. Lumbar lordosis is lost first, then thoracic kyphosis. Typically the neck is spared or involved only later in the disease progression. These patients walk hunched over with a straight back, associated with a lot of discomfort. * Over time, AP x-ray of spine shows squared-off vertebral bodies and loss of intervertebral spaces. This is referred to as bamboo spine or bamboo shoot spine. * We do not know what causes ankylosing spondylitis and we do not have medications to reverse it. * Treatment is NSAIDs (not steroids), physical therapy, IBD treatment if needed, supportive therapy. Reactive Arthritis (Reiter Syndrome) * Patients get an arthritis as a reaction to an infection elsewhere in the body. Infections usually non-gonococcal urethritis (NGU) like chlamydia and infectious diarrheas (campylobacter most common, yersinia, shigella). * Reactive arthritis usually small joints like hand, usually symmetric. * Symptoms include conjunctivitis, oral ulcers, genital ulcers, urethritis. * Mnemonic: “can’t see, can’t pee, can’t climb a tree” for conjunctivitis, urethritis, arthritis. * Blood test to look for in this clinical situation is HLA-B27. * Treatment for NGU reactive arthritis is treat underlying infection and treat arthritis with NSAIDs. * Treatment for diarrheal reactive arthritis is to treat invasive diarrhea cause (prior to getting arthritis). * Do not make the diagnosis of reactive arthritis unless you know what the arthritis is reacting too. Psoriatic Arthritis * Severe destructive erosive changes in the MCP, PIP, and DIP joints. * HLA-B27 positive, more prevalent in men than women. * Symptoms include prominent pitting of the nails, psoriatic skin changes, psoriatic patches on the scalp. Swelling of the fingers can lead to a condition referred to as sausage fingers. * Treatment with some success is methotrexate. Enteropathic Arthritis * Enteropathic arthritis seen with inflammatory bowel disease. * This does follow a similar clinical course to the underlying IBD (ankylosing does not). * Arthritis is typically symmetric, small joints, hands.
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* Sepsis is most often caused by staphylococcus aureus infection or gonococcal infection. Erythema nodosum gets better with treatment of arthritis. An expected response is prompt relief of joint swelling and fever. Causes include sepsis and crystal-induced. He has no prior medical history and takes no medications. All patients that have gout have a predisposition to hyperuricemia. So what are you going to do? NSAIDs now and repeat every few hours. Normally. * Pseudogout crystals are calcium pyrophosphate which is positively birefringent rhomboid-shaped. He occasionally drinks alcohol. trauma from MVC or skiing accident) or hematogenous spread (e. DNA broken down to purines to uric acid. * Gout crystals are monosodium urate which is negatively birefringent (double refraction) needle-shaped. Crystal is yellow when parallel to the slow ray of the compensator. Treatment is several days of parenteral (IV) ceftriaxone. infected IV catheter. * Gonococcal arthritis associated with sexual activity. He has not had recent trauma to his ankle. * Middle aged man with a history of gout tells you to the minute he remember when his foot became painful. What is this consistent with? Gout or pseudogout. so give vancomycin. * Crystal arthritis causes are gout or pseudogout. you cannot make a diagnosis of the cause of monoarticular arthritis. Now what do you do? Answer is polarizing light microscopy. indomethacin). arthrocentesis. the patient doesn’t care about a diagnosis.g. If you do arthrocentesis the next day and the WBC count has not moved. It can be dose-limiting when giving repeated doses. but a very hot gout joint could be 75000. * There are many other causes. Monoarticular Arthritis * Generally a single hot joint presents acutely. * Ankle tap shows WBC of 40.g. the inflammatory response comes way down with NSAIDs (e. if you do find the Gram stain or culture you have a diagnosis (so not very sensitive but very specific). we excrete uric acid into urine (no kidney or liver metabolism). you have the wrong bug or the wrong drug. * Staph aureus gets into joint via direct introduction (e. IV drug abuser. rarely vesicular or pustular) and even tenosynovitis (red streaking along the path of a tendon). Patient put on nafcillin. * Another option is colchicine repeatedly until there is decreased pain. A gonococcal joint implies there has been a bacteremia. safe in pregnancy. The patient should feel better within the first dose or two. even painful swollen hot red.Study Notes – Internal Medicine James Lamberg 28Jul2010 * Treatment should avoid NSAIDs since leukotrienes are pro-inflammatory and bad for IBD. * Another option is short-term steroids.000. * Gonococcal urethritis can be treated with normal dose IM ceftriaxone. But. Treatment is ceftriaxone. Treatment is nafcillin or vancomycin if allergy. A serum uric acid that is normal or low should not rule out the diagnosis of gout. Examination shows red swollen ankle with evidence of an effusion.g. Staph arthritis associated with IV drug abuse. but there are much less common. trauma elsewhere in the body). * Patients with even the most severe acute gouty arthritis might have a normal serum uric acid or even a low serum uric acid at the time they are having their attack. He has noticed his ankle is red. warm. * Most patients with a septic joint. The range of motion is restricted. They have urethritis with discharge followed by a flulike illness with constitutional symptoms then perhaps a fleeting rash (petechial.88 - . If joint space remains inflamed then repeat the tap and the WBC should be coming down day by day if the patient is adequately treated. But. Gout * 32yo man comes in with a history of right ankle swelling that occurred the night before. * Other symptoms include erythema nodosum (painful red nodules on lower extremities) and pyoderma gangrenosum (pus ulcers on lower extremities). and very painful. pink cocci in pairs and chains. * Staph aureus Gram stains positive. Negatively birefringent crystals are seen in association with polys (PMNs) and some crystals inside polys (phagocytized). This is probably nafcillin-resistant staph. * Example would be Gram positive clusters seen on arthrocentesis. so you cannot use the same dose. * Test every time for the first step in the work-up of monoarticular arthritis is arthrocentesis. DO NOT DISTRIBUTE . They came to you to feel better. blue cocci in clusters. Do examination of joint fluid under polarizing light microscopy (for crystals) or do a Gram stain and culture. endocarditis. will have negative Gram stain and cultures. * Neisseria gonorrhea is always hematogenous spread. like Lyme disease. infected central line. * Joint fluid analysis should include WBC count. The problem with frequent high doses of PO colchicine is diarrhea. What is the first step in the evaluation of this patient? Answer is tap the joint. 25-50000/mL in gout/pseudo gout and > 75000 in septic usually. Crystal is blue when parallel to the slow ray of the compensator. * No matter how classic the story is. which implies the patient has had a period of bacteremia where the gonococcus is floating through the blood stream. Best choice though is oral NSAIDs. A WBC < 5000 is more likely traumatic than gout or septic. * Uric acid is a product of nucleic acids from cell nucleus DNA. A day later they spike fevers still and have high WBC on arthrocentesis. * Gonococcus Gram stains negative. but that does not mean it occurs at the time of their gouty attack.
4 Hs: hyperparathyroidism (hypercalcemia). Acetaminophen. Pseudogout * Similar presentation as gout with arthrocentesis WBC in 25-50. * Any patient with DJD who is taking over-the-counter medication should be assumed to be on acetaminophen. He denies constitutional symptoms and other joint pain.000 range. typically lasting less than 30 minutes in the morning. Laboratory testing is unremarkable. * X-rays can show radiodense linear deposits in the articular surfaces or menisci. * If septic joint is in the differential it is essential to do a paracentesis to ensure the joint is not septic. * DJD found in the joint cartilage. again nothing to do with uric acid. so avoid probenecid in this situation. * Disability of patients with DJD is very common. Should you tap the joint every single time? Not necessarily. The last thing you would want to do is put more uric acid in the urine. NSAIDs are effective. such as hips and knees. Then that patient could avoid daily medication with allopurinol or probenecid. When the neutrophils are floating around in the joint space and find a gout crystal. even though it is not truly an inflammatory joint disease. So we have a guy with asymmetric poly arthralgia (not arthritis). this is degenerative joint disease (DJD). He has noticed stiffness in the morning.89 - . diabetes).Study Notes – Internal Medicine James Lamberg 28Jul2010 * Hyperuricemia occurs if you cannot excrete fast enough or you product too much. PIP joint nodes are Bouchard nodes. * Pseudogout associations. You’ve treated this patient for an acute attack and he is back with more episodes. versus RA which affects the synovium. * Say patient has four documented episodes of gout and has limited the major factors you discussed. * DJD is the most common form of arthritis. The most common cause of hyperuricemia is renal insufficiency. hypomagnesemia. sometimes the patient may get diarrhea. typically tumor lysis syndrome. * Do most patients with hyperuricemia develop gout? Probably not. they gang up on the crystals and cause inflammation. * DIP joint nodes are Heberden nodes. it is commonly seen in older patients. * If patient only has gout attack a couple times a year. Another maintenance medication is colchicine. * Probenecid is given to under excreters of uric acid to increase the excretion of uric acid. Only about 10% are over producers. Do we assume gout and treat? No. * There is no medication currently to treat the underlying degenerative process. which are alcohol (uric acid is alcohol metabolite in liver) and purine foods (red meat). Degenerative Joint Disease (DJD) * 64yo man comes to you for the evaluation of knee pain. He says he has had right knee pain for many years but recently it has gotten worse. On exam you hear crepitations when he moves the joints but otherwise there is no evidence of swelling. * Acetaminophen has no useful anti-inflammatory effect. The disease is progressive. This can depend on occupation as well. hypophosphatasia (congenital bone disease). Notice acute gout medications (NSAIDs) have nothing to do with serum uric acid levels. aspirin. * Treatment is the same as gout. it can be seen in anyone who has extensive use of their joints such as an athlete. which is the majority of patients with gout. except for his left second and third DIPs. bone defects. they may be willing to suffer through some pain and take NSAIDs to relieve the attack. but that is not a very good name for the disease. Colchicine prevents this process from happening. warmth. Colchicine is a good maintenance medication for recurrent episodes. hemochromatosis (hyperpigmentation. * Since DJD is a “wear and tear” disease. which reduces the amount of uric acid in the urine. and/or NSAIDs like ibuprofen or naproxen. * Patient has a history of gout and hyperuricemia. plus we give allopurinol to inhibit xanthine oxidase which is an enzyme important to the production of uric acid. hemochromatosis clinical presentation. That is fine in DJD because this is not an inflammatory DO NOT DISTRIBUTE . If you see pseudogout in a younger patient. this is called chondrocalcinosis. 90% of adult patients with hyperuricemia is due to under excretion. * DJD most commonly occurs as an isolated condition due to overuse of joints. Which drug would be best for them? Answer is allopurinol. Now what? Decide if he is an under secreter (give probenecid to cause more urinary excretion) or over producers (give allopurinol to reduce production). * Treatment is aimed at symptom relief. so we give the patients lots of hydration and diuretics if needed to flush the kidneys. * Colchicine inhibits neutrophil chemotaxis. aspirin. Crystals are of calcium pyrophosphate. Look for electrolyte abnormalities. If you miss a septic joint the patient will have rapid destruction of the joint. * Morning stiffness in DJD is short. or erythema of the knee. * DJD also known as osteoarthritis (OA). Whatever causes the patient to have renal failure will result in under secretion of uric acid. * Most commonly affected joints are those used the most. for example a manual laborer may have their hands affected. * Say the gout patient with an inflamed ankle came back 6 months later with an inflamed knee. However. think about the other diagnoses (4 Hs). They begin to develop kidney stones. tap the joint. Predisposing factors are increasing age (more use). * Pseudogout usually occurs in patients older than 50. if the joint is new and it is only the second episode then you should repeat the paracentesis to make sure you do not miss a septic joint.
* Look at urine for RBCs and protein as PAN patients can get glomerulonephritis. Sedimentation rate is very high. Serum blood counts show eosinophil counts of 32%.90 - . Indicated when the patient has intractable pain from their arthritis that cannot be relieve with standard therapies or they are severely disable in terms of function or loss of quality of life. So. diffuse mild abdominal tenderness. low grade fever for several weeks. * Biopsy of the lung or kidney will show vasculitis and granulomas. This is a mononeuritis (one nerve) but multiplex (motor and sensory). * Serology can be positive ANCA (protoplasmic p-ANCA). Churg-Strauss Syndrome * Young person with non-productive cough. knees.Study Notes – Internal Medicine James Lamberg 28Jul2010 disease. * Any older person with constitutional symptoms who develops a new bad headache. What diagnosis is this? This is Churg-Strauss syndrome. Goodpasture syndrome does not have upper respiratory involvement. * Can involve the kidneys with renal insufficiency. The pain is worse when she raises it. You examine the arm and the pulse seems diminished compared to the other arm and femorals. place patient on high dose steroids at the time DO NOT DISTRIBUTE . weight loss. normal chest x-ray. * Wegener granulomatosis affects small vessels. you will see Goodpasture syndrome as both have hematuria and hemoptysis. Henoch-Schönlein Purpura * Patient presents with non-blanching purpura all over their body. and mobilize the joints early to help prevent muscular atrophy. Polyarteritis Nodosa (PAN) * 45yo complains of headaches for several months and worsening abdominal pain after food. Biopsy of purpura shows small vessel vasculitis. * Churg-Strauss is a profound eosinophilic picture with bronchospasm.g. * Goodpasture serology is for anti-glomerular basement membrane (anti-GBM). What is the diagnosis? Answer is Henoch-Schönlein purpura. This is a large vessel vasculitis. * Typically seen in young adults or kids. with stricturing and beading (dilatation). hands. * It is most often seen in young women. * X-ray can show joint narrowing and osteophytes (bone spurs) in any joint involved including spine. The analgesic effect is what we want. There is hypertension and abdominal involvement. The patient complains of abdominal pain with occasional diarrhea. * Diagnosis is made with biopsy of the temporal artery. * Treatment is steroids and immunosuppressive agents if necessary. But. * This is not a common disease but it is one you cannot afford to miss. He also complains of numbness in his foot and weakness with dorsiflexion. showing narrowing of the take-off of various branches of the aorta. * Osteoarthritis/degenerative joint disease by definition does not give a systemic inflammatory response. Temporal Arteritis & Polymyalgia Rheumatica * 65yo with fatigue. * Treatment can include surgical joint replacement of the knee or hip. think temporal arteritis. * Treatment is steroids. wheezing. Now they have a bad headache. recurrent episodes of severe sinusitis. * PAN is inflammation of medium-caliber blood vessels. ice (not heat). * Wegener serology can be positive ANCA (classic c-ANCA). and acetaminophen is safer in regards to renal effects and ulcers. Physical exam shows hypertension. and now has developed hematuria. What is the diagnosis? Answer is Wegener granulomatosis. * Diagnosis made with angiogram. Takayasu Arteritis * Young woman tells you that recently she has arm pain particularly when she uses it for activity. * Treatment for painful joint should include rest. and loss of sensation in the right lower extremity with weakness and loss of deep tendon reflexes in that region. * The complication we worry about is sudden onset of blindness. prednisone). Platelet count and function are normal. Wegener Granulomatosis & Goodpasture Syndrome * Patient has several episodes of hemoptysis. * Every time Wegener is an option. What is the diagnosis? Answer is polyarteritis nodosa (PAN). a common operation. * Takayasu arteritis affects the large vessels/branches of the aorta. * Treatment is steroids (e. sputum shows many eosinophils. * Serology can be positive ANCA (protoplasmic p-ANCA). * Treatment is steroids. Sed rates are very high. This is Takayasu arteritis. * Treatment is steroids and often cyclophosphamide (potent immunosuppressant). Treatment can also include physical therapy. * Churg-Strauss affects medium sized vessels. Biopsy and serology are different.
that is too small a chance so if a patient has pleuritic pain on a board exam question it is not an MI. better when leaning forward or worse with leaning back. Correcting which of the results in the most immediate improvement in outcome? Tobacco smoking. -------------------------------------------------------------------------------------------------------------------------------------------Kaplan Videos (2001) – Cardiology with Dr. Otherwise no one can know the answer. * What is the most common cause of non-cardiac chest pain? Gastrointestinal problems like gastritis. DO NOT DISTRIBUTE . like DVT clot. it’s not like a managed care plan would only allow for you to correct a single problem so you would need to choose the best one to correct. * Which of the following is the most accurate test for her? Well then it might be pH monitor or upper endoscopy. She also has nausea and vomiting. Always associated with a very high sed rate. Wegener. Large vessel vasculitis is temporal arteritis and Takayasu. you can have an MI with no chest pain and with a normal ECG. thus another prominent symptom is jaw claudication with chewing. * Chest wall is non-tender in myocardial infarction. * Any clot or collection of blood can give fever. What is the most common cause of atrial fibrillation in the United States? Hypertension. sometimes when she goes up two flights of stairs. sometimes at rest. pneumothorax (any form of atelectasis). The patient is splitting and does not want to take a deep inspiration. * Myocardial infarction chest pain changes with position 4% of the time. Pericarditis chest pain is positional. with a little chest pain. pneumonia. She also remembers hypertension and hyperlipidemia with low HDL. For boards. if they want you to know an answer they have to tell you something. * Treatment of polymyalgia rheumatic is steroids. hemarthrosis in the knee. But what kind of question is that. Myocardial infarction patient complains of crushing chest pain. subdural hemorrhage. Why not pH monitor or upper endoscopy? To rule out the most dangerous thing first. * Temporal arteritis is associated with polymyalgia rheumatic. Now. They all start with P’s. * Pneumothorax and pulmonary embolism are different from the other pleuritic chest pain in that they are associated predominantly with shortness of breath. It is pain and stiffness of proximal muscles. ruptured ectopic pregnancy. what is the most likely diagnosis in this patient? Answer is ischemic heart disease. Bornholm disease). pneumothorax. often but not always associated with temporal arteritis.e. no evidence of muscle inflammation (no elevated CPK or aldolase). pericarditis. Conrad Fischer. * Small vessel vasculitis is Wegener and Henoch-Schönlein. * Polymyalgia rheumatic diagnosis is made clinical. Chest wall is tender in costochondritis (Tietze syndrome). Do not wait for the biopsy results. cancer. What is the most common cause of hemoptysis? Bronchitis. PE. subarachnoid hemorrhage. Medium vessel vasculitis polyarteritis and ChurgStrauss. She forgot to mention she smoked three packs of cigarettes a day. it is not positional. pulmonary embolism. * 47yo woman now suddenly remember she has had diabetes since she was a child and has been taking insulin for 30 years. etc. Most of the time. The pain has been going on for months. MD -------------------------------------------------------------------------------------------------------------------------------------------Chest Pain * 47yo woman comes to your office complaining of substernal chest pain. EMG would not be abnormal. with a little shortness of breath. duodenitis. Not TB. * Anything that can give pleuritic pain can simulate shortness of breath. Mnemonic is PolyMyalgia and PM for Proximal Muscles. mitral stenosis. But for a board exam. * Fever is not specific enough to differentiate between causes of chest pain. 4% of the time myocardial infarction pain is pleuritic. * Pleuritic chest pain (worse with respiration) causes include viral pleurisy (i. Fever seen in infections and inflammation like pneumonia and pleuritis as well as others like MI. * Quadriceps biopsy of patient with polymyalgia rheumatic would not show inflammation. * What is the most common risk factor for coronary disease and myocardial infarction? Hypertension. What is the most likely diagnosis? Answer is gastroesophageal reflux disease. peptic ulcer disease. etc. these things you would find in polymyositis. esophagitis. She has not past medical history.Study Notes – Internal Medicine James Lamberg 28Jul2010 of suspicion and schedule them for a temporal artery biopsy.91 - . Patient complains of not being able to breath. Devil’s grip. In real life you try to fix all of the risk factors. * What is the best initial diagnostic test for her? Answer is ECG. * Other artery branches can be involved. reflux disease. Goodpasture. * In real life. * Polymyositis is associated with dermatomyositis and the presence of an internal malignancy. * Smoking related deaths are about 2/3 COPD and 1/3 lung cancer. pleurodynia. Oh yea also most of her family members had heart attacks in the 40s and she is a high-stress type A person. sometimes she goes up three flights of stairs and nothing happens. MI clot. It is intermittent and exertional. * Correcting which of the risk factors will improve her long term survival? Answer is correcting all of them.
Even with a history that includes every risk factors. 50 have a non-cardiac problem. For every 100 people who go to the hospital with chest pain. like hypertension (left ventricular hypertrophy) or drugs (patient on digoxin) or pacemaker spike or LBBB? Then do a stress echo or stress thallium test. They are largely based on positional changes. pleuritic. Patient must be able to exercise. < 10% have an MI. or best diagnostic test then pick angiogram. diabetic foot ulcers. * Dobutamine echo stress test abnormalities found by looking for decreased wall motion. ACE-I (if left ventricular dysmotility. * Maximum heart rate = 200 .age. nitrates (no change in mortality).Study Notes – Internal Medicine James Lamberg 28Jul2010 * Sympathetic outflow (diaphoresis. Dobutamine increases contractility and can provoke ischemia. * Reasons to stop a stress test include chest pain. DO NOT DISTRIBUTE . tenderness on chest wall. what does this question mean? You’re being asked what is the next step in management. There is much more muscle in the thighs than arms in nearly all the population. LHV. * Stress echo should look for dysmotility or hypokinesis (decreased wall motion). you will pick up potassium because of the sodium-potassium ATPase. * Sense of impending doom and Levine sign also do not help you determine the cause of chest pain. they just know what is important to listen to. If you are a myocyte in the heart. lightheadedness. The scan will be the same 4 hours later if there is infarct. the capillary cannot delivery the thallium. Tender. what is the best initial diagnostic test? Answer is ECG. If infracted. just as indicated in the equation. Stress Testing & Coronary Artery Disease Management * 47yo lady with intermittent chest pain. Dipyridamole dilates coronary arteries. If you were asked next step in diagnosis then pick angiogram. so increased wall motion normally. Profiling is less accurate. not infarction). congestive failure). hypotension. * 47yo lady is morbidly obese. * Sub-maximal stress test should reach 85% of maximum heart rate: 85% of (220 . 10 have unstable angina. so diagnosis or treatment. Also called a chemical stress test. dobutamine echo stress test can be used when patient cannot exercise. You could memorize digoxin. Now what will you do for her? Answer is cardiac stress test. so more thallium should be picked up normally. An ischemic or infracted area will have decreased thallium uptake. but what if your test has procainamide (causes ST down scooping)? Or some other drug/condition that was not in a list to memorize? Understand the basic question. If there is poor perfusion. you see akinesis (no wall motion). Both have similar indications. dyspnea at rest due to COPD. beta blockers. If there is ischemia. cold and clammy extremities) does not help you specify between causes of chest pain. you want to rule out the most dangerous thing first. pleuritic pain.92 - . and tender. * Real exercise is always better than simulated exercise. Thallium is injected or an echocardiogram done right after walking on treadmill. * Best next step in management for patient with chest pain and ischemic heart disease seen on stress test is medication. both have similar indications. pain. Positional. * In terms of determining the diagnosis. the ischemic portion does not move well during ischemia. has claudication with peripheral vascular disease. They are not smarter than you. * Bicycle ergometry (hand bicycle) is not enough exercise to get the heart rate up. Can she do an exercise stress test? Nope. pale. * Therefore. * Dipyridamole thallium stress test abnormalities found by looking for decreased thallium uptake. just think of things that make it so you cannot exercise. * What if patient has baseline ST segment changes. * Most common cause of death in the United States is myocardial infarction. pacemaker for abnormal baseline ECG. * 47yo lady gets an exercise stress test and it is positive. which is the most important: risk factors or individual presentation? Answer is individual presentation. * How is it that an attending can know about a list of patients while you can only remember information about 2-3 as a new student? It is because they are not listening to most of what you say. Or. No need to memorize the list. it is not as important as presentation of positional. calcium channel blockers (only if patient cannot tolerate beta blockers as beta blockers can decrease mortality and calcium channel blockers do not). shortness of breath. * Thallium looks like potassium to the cardiac myocyte. Give aspirin (lowers mortality). What is the next best step? As a side note. No matter what happens. * Say the ECG is normal. is there a baseline abnormality to the ECG such that I would need to order an echo or thallium stress test? * Dipyridamole (Persantine) thallium stress test used when patient cannot exercise. the area will reperfuse showing thallium uptake. * Major measure of sufficient exercise (test adequacy) is heart rate. you must have the ability to distinguish between the causes of chest pain. doctor must be able to read ECG: look for ST segment depression (ischemia.age) * Exercise tolerance decreases as you get older. and one leg. Pleuritic. How do you tell the ischemia from the infarct if they both have decreased thallium uptake? You re-scan 4 hours later. tachycardia. The attending knows the important symptoms that distinguish between diseases and also knows the most appropriate management.
* Heparin is useful for unstable angina. niacin. * Would giving oxygen help? Not really. total cholesterol. * In a myocardial infarction. * Calcium channel blockers helpful when you cannot use beta blockers or patient has Prinzmetal angina. * 47yo woman with chest pain being treated and LDL is 191. start diet at 160 LDL and drugs at 190 LDL. unstable angina) who has LDL > 130. You do not hear “yea. ST elevation is the best you can do to tell if there is a myocardial infarction now. He is diaphoretic. CABG & PCI * 47yo woman with positive stress test. individual presentation. What do you do next? Answer is statins. VLDL. * Disease. * This is unstable angina because the patient has ST depression. * This is why you hear “he had triple bypass” or “she had quadruple bypass” or “David Letterman had quintuple bypass”. risk factors or individual presentation? Again. * ACE-I only helpful if CHF or decreased left ventricular function. or waist circumference? Answer is LDL. not history. 1 person dies. aspirin. * PCI (angioplasty. oxygen. What is the next step in management? Give aspirin and beta blockers. beta blockers. meaning 3 vessel disease or left main affected. get LDL < 100. Once you have disease. * If ST segment elevation present. * How can you tell now to give heparin or thrombolytics? Answer is ST elevation or not. * What if the patient is allergic to aspirin? Give clopidogrel or ticlopidine. 141? Statins. Surgical mortality is 1%. or fibric acid derivatives. aspirin. The pain goes to his neck and arm. Aspirin and beta blockers reduce mortality. We do not know if triglycerides are associated with disease as well as we know that LDL are related to disease. stenting) if 1 or 2 vessel disease. DO NOT DISTRIBUTE . give heparin. What do you give? Clopidogrel or ticlopidine. Unstable Angina & Myocardial Infarction Management * 64yo man with a history of hypertension and hyperlipidemia comes to the ED with chest pain. Hyperlipidemia * When determining if a patient should get anti-lipid medications. Let the mortality difference drive you. they lyse clots. * Thrombolytics do not lower mortality either. All of those drugs lower total cholesterol and all raise HDL. It’s better to be alive with chest pain. HDL. sense of impending doom. * Risk factors <=1. start statin. diet and exercise is not primary treatment. Better mnemonic is MONAB for morphine. start diet at 100 LDL and drugs at 130. not ECG. ECG shows ST segment depression in V2-V4. If no ST segment elevation. * Diet and exercise only prevent the disease. not cholestyramine. * Patient with coronary artery disease (or MI. a clot is forming and has not occluded the artery. * 47yo woman with positive stress test and aspirin allergy. oxygen. which seems small when it is someone else’s mortality. * How to you differentiate Prinzmetal angina (from unstable angina)? Angiography. although they do not lower mortality they help relieve chest pain. he had single bypass”. She has disease. Levine sign. nitroglycerine. triglycerides. it does not remove the thrombus from the heart and has not been shown to significantly improve mortality. do you look at LDL. * 47yo woman with positive stress test but no risk factors and LDL is 171? Answer is statins. Angiography shows clean coronary arteries for Prinzmetal angina. * Bypass if severe disease. Statins are first. lasting for the past hour. * In unstable angina. * What other medication lowers mortality in addition to the beta blockers and aspirin? Answer is heparin. * Which raises HDL the most? Niacin. angina. short of breath. * For every 100 people who undergo CABG. * Heparin prevents clots from forming. All lower triglycerides as well. start diet at 130 LDL and drugs at 160 LDL. Only aspirin matters there. Thrombolytics do not prevent clots from forming. S4 gallop. why do angiography? To determine if she needs a coronary artery bypass graft (CABG) or percutaneous coronary intervention (PCI) with medications. You won’t be asked diagnosis (unstable angina) or what test to order (ECG). Mnemonic is MONA for morphine. Statins are first because they lower mortality. The patient is not hypoxic in the sense of low arterial PO2.93 - . * Risk factors >=2. * Nitrates and digoxin do not lower mortality. nitrates. What is most important. Thrombolytics is useful for myocardial infarction. give thrombolytics. * CABG is not done for single or double vessel disease because there is no benefit in mortality. a clot has formed and completely occluded the artery.Study Notes – Internal Medicine James Lamberg 28Jul2010 * What is the most accurate test for any disease? Autopsy. it does not matter how many risk factors you have. So when disease is present. Which lowers triglycerides the most? Fibric acids like gemfibrozil. * What else should the man having a possible MI get? Nitrates. Oxygen also given as well as morphine (analgesic) but they are not the most important part. although it is working on occluding.
Use tPA if patient previously got streptokinase. During times of exertion. You are called by the nurse because “he is confused”. Heart exam reveals 3/6 murmur. has cannon a waves. Atropine cuts the brake lines for a while. Thus you leave a meshwork stent “scaffolding” to keep it expanded. * CK-MB and troponins do not begin to arise for 4 hours. Wait. but troponins are even more specific (99. * For MI. * If cardiac tamponade. pulse is 40. Nope. He received all the appropriate therapy. This blocks the parasympathetic. ECG shows ST segment depression in V2-V4. * Myocardial wall rupture with cardiac tamponade would lead to hypotension and confusion. RV infarct and cardiac tamponade could give clear lungs. 40% of inferior wall MIs also have RV infarcts. They saw lightheadedness.9%). thus you would not give these in an acutely bleeding patient. they didn’t have ECG back then. Now what do you do? * What do you do different when you have a major contraindication to thrombolytics and heparin? Answer to open the vessel is do angioplasty. CK-MB (97-99%) is specific. * What is the best initial diagnostic test? ECG. * Complications of an MI can all cause hypotension and hypotension can cause confusion.94 - . LDH is not abnormal from 12-24 hours. do not wait around for enzyme changes. showing complete heart block. Atheromatous plaque gets covered by a little later of endothelium. Valve rupture would regurgitate into the lungs. This is not the right answer though. No hypotension because the blood pressure cuff did not exist then. lasting for the past hour. Which of the following is the most likely diagnosis? * Right coronary artery feeds the right ventricle. heavy periods. causing rales. thrombolytics can be given up to 12 hours from the onset of chest pain (3 hours for stroke). do a pericardiocentesis or a cardiac window then repair the hole. * What about extension of the MI with cardiogenic shock? Not that either. * Transcutaneous pacer makes the heart beat with capture. subarachnoid hemorrhage. described first in 1826 by Stokes and in 1846 by Adams near the University of Dublin. up to a 50% reduction in mortality within the first hour. These are antiplatelet drugs and can make you bleed. may need emergency bypass surgery. * CK-MB last 1-2 days. * Valve rupture with chordae tendineae rupture (after a week) could cause a murmur and hypotension. the plaque ruptures which causes a sudden clot to occlude the artery. epidural hematoma. * If valve rupture. petechiae. because streptokinase can produce antibodies resulting in anaphylaxis. DO NOT DISTRIBUTE . * Glycoprotein IIb/IIIa inhibitors are abciximab. * Efficacy is the same with tPA (tissue plasminogen activator) and streptokinase. Angioplasty is when a catheter is placed through the partially occluded artery then a balloon is expanded to open the vessel. * Most common cause of death immediately post-MI is arrhythmias. but it doesn’t work that way. maybe it is just not up yet since they begin to rise at 4-6 hours and take 12-24 hours to reach peak. Stethoscope invented shortly before by Laennec in France (1816). * Think about what it could be. allowing the sympathetics to work without inhibition and thus speeds up the impulses through the AV node. the management is the same for unstable angina and MI. Post Myocardial Infarction Management * 65yo man in the coronary care unit (CCU) after having an inferior wall myocardial infarction last night. and tirofiban. so why not use lidocaine? Because it does not change the mortality. If they do not change management. * When a patient comes in with chest pain and ECG abnormalities. * 64yo man with a history of hypertension and hyperlipidemia comes to the ED with chest pain. The mortality benefit with thrombolytics is enormous in the first 1-2 hours. may need to go in and emergently replace the valve. bradycardia. * Answer is third degree complete AV heart block. a subdural hematoma. but it also makes all the chest muscles contract. troponins last 1-2 weeks. Patient’s blood pressure is 70/40. We could go to sermons all day long to become saints. Uterus can still make a little CK-MB but no troponins. * All patients who get angioplasty also get a stent to keep the vessel open. * What is the best initial management? Atropine. and inferior wall.Study Notes – Internal Medicine James Lamberg 28Jul2010 * Beside thrombolytics or heparin. but the heart would beat faster to compensate (here the patient has bradycardia). why order them? If the CK-MB is up with ST segment elevation. cannon a waves. The pain goes to his neck and arm. syncope. * Transvenous pacing cannot be setup fast enough and requires an invasive procedure. thrombolytics. Prophylactic lidocaine suppresses those arrhythmias. Overall reduction in mortality with thrombolytics is 25%. * LDH is no longer used in the diagnosis of myocardial infarction. you will still give aspirin. * Also. * Cardiogenic shock would give rales. If CK-MB not up. Troponin I is the most sensitive and specific. * If cardiogenic shock and extension of the MI. a chest that is clear to auscultation. But no. It is like a car that has an accelerator (sympathetics) and brakes (parasympathetics). thrombolytics dissolves the clot then give heparin afterwards to keep it open. The problem is when you remove the catheter the plaque can bulge back out. beta blockers. This patient has a clear lung auscultation exam. eptifibatide. He has melena. AV node. Lidocaine also causes arrhythmias.
now you may have lost 40-50% of your cardiac output because you need the atrium to push blood forward. * ACE-I will decrease mortality in the long-term. enlarged spleen. and alcoholic cardiomyopathy. loop diuretics. Dobutamine decreases the afterload. edema to waist. * Dopamine is only used if you need to raise the blood pressure. radiation to her heart and chest. so you have a weak leaky heart. * There are many causes of CHF and the initial diagnostic tests and management are all the same. but we know all this. 80-90% of patients will get better with this therapy. Which do you give for this patient though? Dobutamine. If you have an intractable dry cough. it does not change management. myocardial infarction (more ischemia). but more accurate than an echocardiogram. * Valvular rupture occurring a week after an MI would cause regurgitation leading to acute pulmonary edema. It is only used as a pressor here. * Dopamine and dobutamine are both positive inotropes. hypertension. Patient comes in short of breath saying they feel like they are filled up with fluid. and thus does not change blood pressure. But that is because your heart is not weak (cardiomyopathy). Preload reduction will save this patient’s life. give an ARB (-sartan drugs. * If you have congestive failure and you develop atrial fibrillation. They will both increase contractility (positive inotropes) and myocardial oxygen consumption. ethacrynic acid. stroke volume to be precise.95 - .Study Notes – Internal Medicine James Lamberg 28Jul2010 Congestive Heart Failure (CHF) * 67yo woman with a history of MI. * Say you give this patient oxygen and preload reduction but she is still short of breath. * What is the most common cause of developing congestive heart failure in the United States? Post-MI. These patients need atrial contribution. The difference in this measurement corresponds to the ejection fraction. Since it is nuclear energy. pulmonary vascular redistribution. They die from pulmonary edema. but not the most accurate test. * Many years ago before IV furosemide was around physicians did phlebotomy and rotating tourniquets. * Patient will not die from lower extremity edema or organomegaly. but she already knew that and she doesn’t care. what is the next best step in management? Answer is oxygen then loop diuretics. This is dilated cardiomyopathy. effusions. But you know this. * Most accurate way to measure ejection fraction is MUGA scan. The fastest was to get fluid out of your body is diuretics. Echo is the best initial method of measuring ejection fracture. * ABG would show hypoxia and low CO2 (hyperventilating). adriamycin use. You could look at a soda bottle and take a cross sectional diameter to get an estimate of the amount of soda inside. like losartan or valsartan). * ARB drugs are angiotensin II receptor blockers. JVD to ears. and that is what a MUGA scan is about. beri beri. * There needs to be an event causing (acute) pulmonary edema in a patient with underlying CHF. S3 gallop. morphine. * How much cardiac output is based on atrial contribution? Answer is 10-20% in normal person. nitrates. Getting fluid out of the lungs now will help reduce preload. * Nitrates also work at pre-load reduction because they dilate both arteries and veins. Kerley B lines. DO NOT DISTRIBUTE . but dilate veins more. torasemide. also known as systolic dysfunction. * 67yo woman with CHF and now acute pulmonary edema. worsening the congestive failure. ascites. She says she has shortness of breath while laying flat but feels better when she goes to the window and puts her head outside (what makes her feel better in reality is just getting up). * MUGA scan is a nuclear ventriculogram (radionuclide ventriculography). The goal now is to decrease afterload. valve disease. Loop diuretics are furosemide. They are cheap. * Loop diuretics are used because they are intravenous and work fast on the ascending loop of Henle. dead (post-MI). Common causes are stopping medications. Nuclear isotope is injected into the body and the scan measures the amount of nuclear energy emitted from the heart in diastole and systole. * Catheterization and angiogram is less accurate. clean. Most common adverse reaction to ACE-I is cough and hyperkalemia. Wall motion gets worse when your heart becomes ischemic. But the better way is to pour fluid into the bottle and measure how much actually comes out. Chagas disease. Give her medication for her shortness of breath and to reduce preload: oxygen. enlarged liver. and hemorrhoids. She comes in while chowing down on an entire pizza. easy. leaky (valve regurgitation). * Dopamine increases the afterload. arrhythmia. give loop diuretics. weeks to fully take effect. * CXR would show enlarged heart with congestion. This patient has lungs filled with fluid and thus is not oxygenating. * Morphine can reduce pre-load as well. Presentation is dyspnea with rales to apices. * The least accurate method to assess ejection fraction is an echocardiogram. That’s great doc. * Why not use digoxin now since it is a positive inotrope? It takes time. * For this 67yo patient. increased salt load. A CXR does not change our management in this patient. it is not based on a cross sectional diameter like an echo or catheterization. bumetanide. * Afterload reduction is best achieved with ACE-I (-pril drugs). What are you going to do to help her is the question. Myocardial infarction killed off part of the heart. You do a CXR and tell her that her lungs are filled with fluid. So you can live without the atrial kick. but they will not help acutely. You will not be asked the diagnosis here. which is CHF in its worst form called pulmonary edema.
Don’t forget the even less common Lighthouse sign. it will be too late. diuretics. and beta blockers. Sherman sign. Lincoln sign. That thing is that they do not die. do you cut out a piece of underwear to fix the size? No. You give potassium if the patient is only on diuretics and digoxin. Duroziez sign (systolic and diastolic murmurs described as 'pistol shots' heard over the femoral artery when it is gradually compressed). Gerhardt sign. Sometimes you may need digoxin. When your butt gets really big and your underwear stretches. what is the most important medication to discharge her on? Answer is ACE-I. and that is why beta blockers are good as they lower heart rate and cardiac contractility. reactive arthritis. angina. furosemide. * What is the most common cause of mitral stenosis? Rheumatic fever. Becker sign. S3 gallop. Traube sign (a double sound heard over the femoral artery when it is compressed distally). When you lower the heart rate you reduce ischemia and the patient is less likely to die. but it can cause any valvular disease. Basic sciences in medical school will tell you over and over that beta blockers are negative inotropes that worsen ejection fraction and worsen cardiac output. Batista partial ventriculectomy). Also. if you plan to replace the valve you should not wait for the heart to dilate up in size. * Exotic findings for aortic regurgitation are largely archaic. * Mitral stenosis is the most likely valvular disease to have hemoptysis. they increase ejection fraction and cardiac output. * Diuretics and digoxin have not been show to lower mortality. syphilis. * What is the bigger problem in cardiac failure with systolic dysfunction. angina prognosis is 5 years. Hill sign.Study Notes – Internal Medicine James Lamberg 28Jul2010 * 67yo lady with pulmonary edema and CHF was treated with oxygen. Infarction can cause regurgitant lesions through this mechanism. Marfan syndrome. the weak heart or the ischemia? Ischemia. Rosenbach sign. heart transplant needed. * The ease of availability and use of the echocardiogram has led to a decline in our ability to auscultate murmurs. These all added together and multiplied by 10 are still not even close to causes of aortic regurgitation compared with myocardial infarction and dilation of the heart. Going back to stress testing. * When your heart dilates. Hearing a diastolic murmur is more reliable. * Aspirin has been shown to decrease mortality in coronary disease but not congestive failure. HLA-B27 stuff. Anything that dilates the heart has to cause regurgitation because the leaflets separate. because the ostia (entry points) for the coronary arteries are distal to the aortic valve. Corrigan pulse (rapid upstroke and collapse of the carotid artery pulse). the valve leaflets do not change in size. * There is an interesting thing that happens to patients with congestive failure who are on beta blockers and they like it quite a bit.g. There can also be hoarseness as the atrium presses against the recurrently laryngeal nerve. and Ashrafian sign. She feels all better the next day. atrial fibrillation (with emboli to brain).96 - . as the diuretic would make you hypokalemic and the digoxin would then become toxic. de Musset sign (head nodding in time with the heart beat). you need an underwear transplant. dyspnea (CHF). ACE-I has been shown to improve mortality. * Aortic stenosis is associated with syncope. morphine. * What can be done to restore a heart to normal shape and size once it dilates? Nothing. * But won’t beta blockers worsen ejection fraction? Actually. Landolfi sign. * These exotic findings are usually only seen in longstanding non-treated disease. Worse prognosis is with CHF. * ACE-I can raise potassium and help offset diuretics.g. Müller sign. what is the major determinant of exercise? Heart rate. * What else causes mitral stenosis? Congenital. Ehlers-Danlos. Mayen sign. but they do not alter anatomical heart size. Valvular Heart Disease * Valvular disease is organized into stenosis and regurgitation. Cardiomyoplasty. 1-2 years average until death. nitrates. * Fundamental symptom of all valve disease is CHF (rales. * Infections (e. * Rare aortic regurgitation causes include ankylosing spondylitis. and dysphagia. but not a regurgitant loose/floppy lesion. The actin and myosin filaments have become separated and cannot contract well. That was because beta blockers had not been studied in congestive failure because everyone thought it would make things worse. thus another cause of angina. Syncope prognosis is 3 years. * Since nothing can be done after the heart dilates. Dysphagia because the enlarged left atrium (most posterior heart structure) presses on the esophagus. The echo has greater sensitivity and specificity than the stethoscope. more than by valve location. * Calcification can cause mitral stenosis and aortic stenosis. * ACE-I may stop the dilation problem from getting worse. DO NOT DISTRIBUTE . like Watson water hammer pulse. None of these have utility in making a diagnosis. Most common symptom of aortic stenosis is angina. edema). but it can cause any valvular disease. does not work (e. slicing a piece of the dilated heart out. endocarditis) can cause regurgitant lesions from vegetations. We replace the valve before these patients join the American Iatrogenic Association. CHF. If you wait. because they are antiischemic. Quincke sign (pulsation of the capillary bed in the nail). Mnemonic: SAD for syncope. but not stenotic lesions. and angina. * Beta blockers lower mortality more than ACE-I in congestive failure. coronary artery disease is common in patients with aortic stenosis (older men). The stenotic aortic valve blocks blood flow into the coronary arteries.
* Squatting maneuver increases preload. Valve replacement with vessel bypass is the therapy. Digoxin will not help because it helps blood squeeze out of the ventricle. * Do not give beta blockers to AS. Why? Plasma volume goes up but the size of the mitral valve does not. and MR. and afterload reduction. She delivers here baby but still has bad shortness of breath despite diuretics and salt restriction. What is the next best step in the management of this patient? Balloon valvotomy. But what can you do in the meantime before replacing the valve. This makes it easier for blood to get out of the heart. But this is very invasive. When a patient exercises. 5mmHg laying flat. the heart contracts more completely causing more obstruction. Panic attacks. Valsalva). pulmonic at upper left sternal border. Murmur will increase with more blood in heart (leg raise. Do not give HOCM or MVP patients diuretics. * Aortic stenosis calcifications are from calcium. thus balloons do not work as well. Mnemonic: Prolapse. Most common cause is congenital. positive inotrope. Exhalation against closed glottis. is valve replacement at the top of your list for management? Lets hope not. ACE-I and vasodilators are the most important. * Mitral stenosis treatment includes preload reduction (diuretics. Treatment is preload reduction. * Mitral stenosis (MS): opening snap moving closer to S2 as stenosis worsens because left atrial pressure increases so it pushes the valve open earlier. * Leg raising increases preload. mitral at lower left midclavicular area. salt restriction). * Transthoracic echo (TTE) or transesophageal echo (TEE) first? Answer is TTE first. which increases intrathoracic pressure and decreases venous return to the heart. Murmur will increase with more blood in heart (leg raise. Decreases with preload reduction (standing. palpitations. * Aortic regurgitation (AR): decrescendo murmur because blood gets shot up out of the aortic valve and you do not hear anything. Valsalva). * Occasionally a myomectomy is needed for HOCM to remove the obstruction. Best initial therapy for HOCM is beta blockers because it decrease the heart rate thus more filling and thus less obstruction. Cardiac Auscultation * Auscultation locations are APTM (“all physicians take money”). There is no pressure pushing blood back into the heart. Have patient bear down like they are having a bowel movement is another way. there is more murmur with less blood and less murmur with more blood. * 27yo pregnant woman with much worse symptoms from her mitral stenosis. MR because it would make the murmur/problem worse. Most common presentation is dyspnea. * Mitral valve prolapse (MVP): mid-systolic click due to leaflets stopping short. Treatment is valve replacement if symptoms persist. If you increase the intrathoracic space pressure (valsalva) it pushes blood out of the thorax. pansystolic or holosystolic murmur. that is the question. MS. * Aortic stenosis (AS): crescendo-decrescendo murmur. AR. * Valsalva maneuver decreases preload. * With balloon valvotomy a vascular catheter is threaded across the valve and a balloon dilates. DO NOT DISTRIBUTE . squatting). so anything that makes the heart larger (more blood) pushes away the obstruction and decreases the murmur. * Standing suddenly decreases preload. the heart empties more fully causing more obstruction. opening the valve. * Mitral regurgitation (MR): S1 and S2 are obscured by constant murmur. * Commissurotomy would help increase the size of the stenotic hole. * Hypertrophic obstructive cardiomyopathy (HOCM): crescendo-decrescendo murmur. then you hear the blood crashing down on the ventricle. Leg veins are compressed pushing blood up into the heart. * Mitral regurgitation and aortic regurgitation are managed with the same medications used for CHF. Which is best? TEE. * Right atrial pressure when sitting is zero. Presentation is most commonly pain (atypical chest pain). AR. Valsalva). Palpitations. * The ultimate step in management for all valvular heart disease is replacement of the valve. balloon valvotomy does not work well. Digoxin. When dehydrates. * ACE-I help get blood out of the ventricle. Asymmetric septal hypertrophy is in the way. blood basically just falls into the right atrium. * Cardiac catheterization is the only way to get direct pressure readings for any valvular disease. It is the most common cause of sudden death in healthy young athletes. Digoxin would help with atrial fibrillation because it helps decrease the heart rate and ventricle fills during diastole. * Note treatment and maneuvers are the opposite in HOCM and MVP compared with AS. Initial therapy is beta blockers. Decreases with preload reduction (standing. panic attacks.Study Notes – Internal Medicine James Lamberg 28Jul2010 * Initial test of choice for any valvular disease is echocardiogram. Blood is brought away from the legs and into the heart. Decreases with preload reduction (standing. and we do not have a problem with that in mitral stenosis. Pain. * With aortic stenosis. when standing it could be almost sub-atmospheric. If the porcine valve needs to be replaced every 10 years and we have a 27yo pregnant female here. and ACE-I would thus cause more obstruction. Valsalva). upper right sternal border. How do you get the valve into the heart? Open heart surgery in general with median sternotomy. MS. squatting). lower left heart apex. Unlike the other murmurs of the left heart.97 - . aortic at upper right sternal border. tricuspid at lower left sternal border. blood pools in the legs so less blood in the heart. diuretics. Decreases with preload reduction (standing.
* Inflammatory causes include SLE. DO NOT DISTRIBUTE . rheumatoid arthritis. but you can bundle any one of the causes into these main topics. * Causes of pericardial tamponade are the same as pericarditis. * Constrictive pericarditis symptoms are JVD. * Trauma causes include open heart pericardiotomy trauma. chest wall trauma. cytomegalovirus. Pathognomonic ECG finding is PR segment depression. * What occurs in constrictive pericarditis that does not occur in CHF. * What about peritonitis? Yep. so how do you distinguish? Answer is pulsus paradoxus and clear lungs. rheumatic fever. * Causes of pericarditis include tuberculosis. syphilis. and fibrosis. * Normal heart rate of 60 to 100 is based on thousands of military recruits between the ages of 18 and 24. * Causes of pericardial tamponade are pneumonia. & Pericardial Tamponade * Beta blockers are not used in restrictive cardiomyopathy because it is not hypertrophic. Dressler syndrome. ascites.98 - . * First test of choice is echocardiogram. What are you going to learn from this? Pretty much nothing. Heart rate is seen on ECG. give atropine acutely to increase the heart rate then a pacemaker later on. By the 20th item on the list the audience will look like the old Maxell tape ads with the guy in front of the speaker being blown back. Try to do this for any disease with a long list. uremia. Sjögren syndrome. Viral is the most common. standing). pneumococcus most often. while the medical students will look at each other and say “Uhh. what you would be expected to managed as a physician intern at a hospital. and hypotension. * Causes of restrictive cardiomyopathy include amyloidosis (protein accumulation from inflammatory disease). rickettsia. What is the next best step in management? This patient does not have symptoms so ECG. * Say you’re in a lecture and someone is listing all the causes of pericarditis. ACE-I and diuretics are not used because it is not dilated. Thus all left sided murmurs get more intense with more blood (leg raise. * Treatment is to remove the pericardium. esophagus. * Treatment of pericarditis is to correct the underlying etiology. yep stop cause it’s any trauma. toxoplasmosis. inflammatory. enlarged liver. same causes there too. klebsiella. strep. * What are the causes of pneumonia? Anything. * Side note. * ECG shows ST elevations everywhere. Any major textbook will list these items in completeness. * 47yo man comes to the office seeking advice about diarrhea prophylaxis prior to going to a vacation to Thailand. So what do you do to treat a chronic pericardial effusion? Pericardial window. a hole in the pericardium and fluid drips into pleural space. pulse rate is not the same as heart rate. cancer. * Cancer causes include. trauma.. wanna go get a beer?” * There are over 50 separate causes of pericarditis. Pericarditis. It does not matter how low it gets because he has no symptoms. * Chronic pericardial tamponade becomes constrictive pericarditis from fibrosis. pseudomonas. * Sinus bradycardia at a rate of 47 in an asymptomatic man. If NSAIDs do not work. it’s any cancer near the heart. squatting) and less intense with less blood (Valsalva. And pulmonary contusion with atelectasis leading to pneumonia. * CXR or CT for diagnosis. coxsackie). tachycardia.yea no point. NSAIDs. * Treatment of choice is needle pericardiocentesis. If he did have symptoms. Infections. staph. anaerobes. Restrictive Cardiomyopathy. What if the heart rate was 37 without symptoms and ECG showing sinus bradycardia? Do nothing. * Can trauma cause a pleural effusion? Yep. Arrhythmia Management * The type of arrhythmia management that you need to know is the first hour of management.g. All the attendings and residents who know the lists will love the ever so complete lecture. mixed connective tissue disorder. * Which connective tissue disorders have pulmonary involvement? Any connective tissue disorder. then use prednisone. sarcoidosis. * Symptom of pericarditis is pain that is positional and pleuritic. scleroderma. Exceptions are HOCM and MVP. * Presentation is jugular venous distension (JVD). pleural effusion. But that could be pulmonary edema. then a Valsalva will make the murmur less intense by the same concept of preload reduction. yep any connective tissue disorder or inflammatory disorder. Gram negatives. viral (e. If no etiology (mainly viral). * The problem with the pericardiocentesis is that the fluid can keep re-accumulating. next step is leave him alone. Pericardial knock. Lungs.Study Notes – Internal Medicine James Lamberg 28Jul2010 * If a diuretic is used to treat a murmur (preload reduction). mediastinal lymph nodes are all near the heart. pulse is palpated. * What cancer can affect the lung? The ones that are anatomically near the lung. pleuritis. breast. You notice that he feels alright but his heart rate of 47. hemochromatosis. yep anything. two hours post prandial in the supine position. cancer..
* Survival without defibrillation declines to zero after ten minutes. and beta blocker in this scenario are the same so it does not matter. This does not progress to second degree AV block. Chest compressions do not restart the heart. 40% of your patients just died since 10% are lost per minutes. this can progress to complete block and ischemia. is at an important dinner in Japan. mammalian dive reflex (mostly for kids. Adenosine only used for SVT. suction. What is the next best step in the management of this patient? If stable. * 28yo female medical student who has been preparing for an exam and using the four basic food groups.Study Notes – Internal Medicine James Lamberg 28Jul2010 * First degree AV block without symptoms do nothing. caffeine. Now what? Defibrillation. * Say ECG shows up and patient is in Vfib with no respirations. * Say patient is truly unresponsive to even painful stimuli. * Conduction jelly is used to increase the surface area for the shock and to decrease the burn because dry skin burns. Eyeball massage can cause retinal detachment and it is not needed. calcium channel blocker. * Does that mean a person with a normal systolic blood pressure of 88 gets shocked in this situation? Yes. * 72yo former president of the U. * Mobitz type I AV block (Wenckebach) without symptoms do nothing. He is found to have ventricular tachycardia (Vtach). so don’t do that. The indications for digoxin. Determine if the patient is responsive and not just sleeping. beta blockers because it will block the effect of the sympathetic outflow from the hyperthyroidism. Open airway. calcium channel blocker.and blinding the patient. atrial flutter (Aflutter). Call for help before moving on to the rest of the algorithm. * Say patient had a history of asthma? Then do not use beta blockers because it could cause bronchospasm. * Coumadin is used when patient has chronic atrial fibrillation. What is the next step in management? Call 911. Blood pressure is 128/88. This does not usually progress and is part of the normal aging of the conduction system. DO NOT DISTRIBUTE . or confusion.g. ventricular fibrillation (Vfib). If unstable. Valsalva maneuver. check pulse. do synchronized cardioversion. Because after you have had Afib for more than two days you are at risk for emboli. alcohol. nicotine. What does unstable mean though? Hemodynamic instability means systolic blood pressure < 90. adenosine. unstable gets defibrillation. he has no pulse so we start compressions. What is the next best step in the management of this patient? * Does he have hemodynamic instability? No. ECG shows supraventricular tachycardia (SVT) at a rate of 160. American Heart Association has spent a great deal of time working the algorithm out. check breathing. beta blocker. he has lightheadedness and confusion. After ten minutes without defibrillation. pulseless electrical activity (PEA). chocolate. * 57yo man at the opera who gets up. * Stable patient with SVT and vagal maneuvers did not work. gets up to make a point. She comes in complaining of palpitations. beta blocker. calcium channel blocker. how long would it take to intubate in the field? Maybe 3-4 minutes with getting equipment out. * Mnemonic for SVT meds: ABCD. becomes lightheaded and confused. * Determine if the patient is unstable. atrial fibrillation (Afib). SVT) first step is vagal maneuvers like carotid sinus massage. * 57yo man at the opera who gets up. give two breaths if not breathing. chest pain. asystole. In that time. the patient has no good chance of survival. There is a 10% decline in mortality per minute. circumferential digital rectal examination. you better be sure about the next step of management. shortness of breath. Not intubation. We have to agree on a definition for hemodynamic instability. Thus. or digoxin. they keep you alive while waiting for the important equipment (defibrillator) to arrive. then slow the rate. How do you know which one to use? These all slow the rate but do not convert the rhythm. Say we skip this step and open the airway. * Say the patient is unresponsive and pulseless. You can give digoxin. leans forward and vomits all over the Japanese ambassador. * Eyeball pressure does a good job of slowing the heart rate. * Rate controlling meds for non-SVT atrial arrhythmias are BCD: beta blocker. He is found to have rapid atrial fibrillation secondary to Graves disease. What is the next best step in the management of this patient? Answer is determine if he is conscious or unconscious. * Stable patient atrial arrhythmia (e. calcium channel blocker. you better call for help to get the equipment there so you can distinguish these.99 - . What’s the problem now? Well.. which means > 48 hours. falls to the floor and is not moving. ice back to face). We do not wait for the patient to have their first syncopal episode while they are driving down the road. What is the first step in management? * Multifocal atrial tachycardia includes SVT. then you do ABCs. * Mobitz type II AV block is the dividing line. digoxin. do a couple of rescue breaths.. start compressions if no pulse. no one is coming to bring a defibrillator or take this man to the hospital.S. and get the tube in. then adenosine. What is the only way to distinguish these? ECG. * After calling for help. Thus. * Mobitz type II AV block and type III complete AV block get a pacemaker even without symptoms. What is the differential? Pulseless ventricular tachycardia. * If vagal maneuvers and adenosine do not work. They are all the same in their management except adenosine. * Vtach that is stable gets lidocaine.
atropine and epinephrine can be given between CPR cycles.Study Notes – Internal Medicine James Lamberg 28Jul2010 * If defibrillation did not work. They become unconscious and the ECG shows flat line. not uncommon. Each large box is 200ms. so it might not be perfectly flat line. You consider pacemaker because it could possibly be very slow bradycardia and you may have missed a beat. The patient states DO NOT DISTRIBUTE . etc. the patient is dead anyway. Defibrillation stops the heart with the hope that it will reboot normally. maybe two or three. do a cycle of CPR then shock again. You can differentiate tachycardia from bradycardia this way. atropine is 1mg for cardiac arrest and 0. * Say you’ve given epinephrine and atropine through several cycles of CPR and the patient is still dead. * 300 method points are 300. it will not help. * Know what ventricular fibrillation looks like and do not expect Torsades. * Magnesium is given for Torsades de Pointes only. there is nothing else to do. Wide complexes are > 120ms. After three cycles with refractory VT or Vfib. Irregular waves with no consistency across the rhythm strip. Count the number of large boxes between QRS complexes and divide 300 by that number. * What about the dosing of these drugs and shocks? Drug dosing is not asked on board exams. * Consistent wide complexes is ventricular tachycardia. Side note: always confirm asystole in a second lead. drug. Don’t think something like the leads came off the patient’s chest. precordial thump used in witness arrest only with no defibrillator present. What is the best next step in management? CPR. She has the defibrillator ready and is asking you what to do. which makes them narrow on the QRS. * ECG showing flat line. Exception may be the advanced cardiac life support (ACLS) drugs here. Defibrillating asystole will do nothing because the electrical system is already stopped. Couplets are two PVCs. * Intracardiac medication has not been show to have greater efficacy so it is not an answer. 50. The amount of energy needed for successful defibrillation is little at the very beginning. then epi and atropine for a few rounds. CPR. * Each small box is 40ms. drug. Four or more is ventricular tachycardia. * Resuscitation of patients beyond 10 minutes only in hypothermia or induced hypothermia. use that instead. * Bigeminy is every other beat being a PVC. * Arrhythmia associated with digoxin toxicity is bigeminy. Precordial thump is like defibrillation and you do not defibrillate flat line. One is PVC. Epinephrine can be given between each cycle as well. What do you do next if the patient is conscious and stable? Give lidocaine. The most common arrhythmia seen in digoxin toxicity is SVT with variable block. * Precordial thump is like a little defibrillation.100 - . You feel a pulse and note that it is 70 per minute. There is some biological variability. What do you do? Defibrillate. What medication can you give for refractory VT or VF? Amiodarone. Should you do a precordial thump for the witnessed arrest? No. 100. adenosine is 6mg to start. 75. CPR. this does nothing. Epinephrine is 1mg. 10-20J of energy. You can consider a pacemaker. QRS should be less than 3 small boxes (120ms). * ECG shows Vfib and you’ve gone through cycles of CPR with defibrillation. then consider a pacemaker. * Do not shock asystole. 150. any arrhythmia. it’s not like jumper cables for a car. * Supraventricular can be differentiated from ventricular by the width of the QRS complexes. Thus. Algorithm says consider because beyond that you are considering burial or cremation. * For asystole or PEA. then consider the patient dead. How much time do you have to save this patient? 10 minutes. Two is couplet. For true asystole. Wide complexes always comes from the ventricles. If you have a defibrillator. So shock. * Thoracotomy with direct cardiac massage is also not an answer. 60. Now you intubated the patient and give epinephrine during the cycles. Patient is always pulseless. * Ectopic beats originate from an ectopic focus. lidocaine is 1mg/kg.5mg for bradycardia. it’s more like rebooting an electronic device when it is not functioning well. This is asystole. Electrocardiograms * There are very few ECGs on USMLE Step 2. * You are at the bedside for a patient with chest pain. * What if ECG shows Vtach and patient is unconscious? Defibrillation. * PR interval should be less than 5 small boxes (200ms). shock. * Counting rate is done by the 300 method. Three is triplet. Supraventricular impulses follow the normal conduction pathway through the AV node. amiodarone is 300mg. It may be important to know the most common wrong answer in situations like this because both will be listed on the exam and likely they are the two answer choices you narrow down to. * Important Note: There is no minimum and no maximum for running a resuscitation. So if there were 5 large boxes between QRS complexes it would be 300/5 = 60bpm. * You get called into a room by a nurse because the monitor shows the patient’s rate at 140 per minute. CO2 production of each cell and oxygen consumption is directly proportional to body temperature. you can give amiodarone or lidocaine. trigeminy.
The peaked T-waves are so high that the monitor is reading them as QRS complexes.101 - .Study Notes – Internal Medicine James Lamberg 28Jul2010 she missed her dialysis treatment this week. then the exam will feel smaller and your process will be filled with more joy. If you are conscious of the goodness that comes from the knowledge after that and what it can do to be of service. if your highest point to attain is the exam it will feel painful. What could it be? Hyperkalemia. * Keep in mind when you are studying for the exam. The pointier the worse. the size does not matter as much as the shape. * The most important ECG to know is regular sinus rhythm. * When talking about peaked T-waves. -------------------------------------------------------------------------------------------------------------------------------------------- DO NOT DISTRIBUTE .
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