Study Notes – Internal Medicine

James Lamberg

28Jul2010

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.

DO NOT DISTRIBUTE

-1-

Study Notes – Internal Medicine

James Lamberg

28Jul2010

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

DO NOT DISTRIBUTE

-2-

Study Notes – Internal Medicine

James Lamberg

28Jul2010

* 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.

DO NOT DISTRIBUTE

-3-

and fasting hyperglycemia. or gender. 8) A key concept in evaluating patients with hyperfunctioning endocrine tumors is that biochemical diagnosis should always precede anatomic localization. hypertriglyceridemia. 7) Pituitary tumors cause problems for patients by two main mechanisms: mass effect. 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. which applies pressure to surrounding structures. 17) In patients with Coccidioides immitis infections. 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. elimination of secondary infections. low HDL cholesterol levels. 2) Acute pulmonary embolism (PE) is a difficult diagnosis to establish despite newer advances in imaging. early targeted and specific drug therapy. regardless of the blood low-density lipoprotein (LDL) cholesterol level. and endocrine hyperfunction. effective antimicrobial therapy. higher titers of complement-fixing antibodies suggest more extensive disease. 13) The goal blood pressure is < 130/80 mmHg in hypertensive subjects with diabetes mellitus and/or chronic kidney disease. approximately 50% of cases are diagnosed post mortem. 6) Metabolic syndrome is diagnosed on the basis of abdominal obesity. The one exception is patients with pituitary/hypothalamic dysfunction. 12) Diabetics and patients with vascular disease should be treated with a statin lipid-lowering drug to prevent heart disease and stroke. 3) In the approach to suspected PE. 11) All patients with coronary artery disease (CAD). age (from 40 to 79 years). 10) The most common presentation of hypogonadism is erectile dysfunction and decreased libido in men and amenorrhea and infertility in women. 4) The most common etiologic agent implicated in acute bacterial meningitis in the U. 21) In patients with disseminated candidiasis. DO NOT DISTRIBUTE -4- . in addition to routine adult immunizations. immunizations against pneumococcal pneumonia. which results in excessive secretion of a particular anterior pituitary hormone. in whom TSH cannot reliably to assess thyroid function. 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. euglycemia. IV catheters should be removed and ophthalmologic examinations performed to evaluate for the presence of retinal disease. 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). 5) In the newly diagnosed HIV patient. and rising titers suggest worsening disease. 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. and establishment of therapeutic goals. and both hepatitis A and B are indicated.Study Notes – Internal Medicine James Lamberg 28Jul2010 -------------------------------------------------------------------------------------------------------------------------------------------Top 100 Secrets – Medical Secrets (4th. hypertension. keep in mind the prudent use of key diagnostic tests: (1) rapid d-dimer by ELISA is an effective screening test. 18) Patients who present with flaccid paralysis during the summer months should be evaluated for West Nile virus infection. and (3) a negative Doppler venous ultrasound of the legs does not exclude the diagnosis of PE. or diabetes should be treated aggressively to reach the LDL-cholesterol target of 100 mg/dL. is Streptococcus pneumoniae.S. influenza. 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. since it is the most sensitive measure of thyroid function in the majority of patients. 9) The best initial screening test for evaluation of thyroid status is the TSH. CAD-equivalent diseases. (2) chest CT can help detect most PEs.

there is a high chance of superior vena cava obstruction. especially in younger (< 20 yr) or older (> 70 yr) patients. hypokalemic metabolic alkalosis. and fluctuating neurologic signs suggests thrombotic thrombocytopenic purpura (TTP). metabolic acidosis. 27) About 90% of patients with primary sclerosing cholangitis have underlying ulcerative colitis. 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. but correction of iron deficiency and iron supplementation by oral or intravenous route is simpler. secondary to juxtaglomerular hyperplasia. and calcium oxalate crystals in the urine. especially if they continue to smoke and drink. 45) Hyperkalemia is an important side effect of both ACE inhibitors and ARBs. 50) The cytogenetic marker of chronic myelogenous leukemia is the 9:22 translocation. 46) Hypochromic microcytic anemias are the most encountered anemias in hospitalized and ambulatory patients. 33) Patients with head and neck cancer have a 30% chance of developing another cancer somewhere in the aerodigestive tract (head and neck. 43) Ethylne glycol (antifreeze) toxicity is characterized by high anion gap metabolic acidosis. and foramen of Morgagni (rare). 42) D-lactic acidosis is characterized by increased serum anion gap. the minimum amount of free air that can be detected on an upright chest x-ray is 12mL. lung. the chance of developing breast cancer can be reduced by about 50% with the use of tamoxifen. GI bleeding stops spontaneously in about 80% of patients. In iron-deficiency anemia. 38) Treatment of anemia of chronic renal failure by recombinant human erythropoietin is highly effective. a sign of mediastinal involvement (recurrent laryngeal nerve) that renders the patient inoperable. perform a biopsy. prophylactic cholecystectomy is recommended.Study Notes – Internal Medicine James Lamberg 28Jul2010 23) Porcelain gallbladder is an incidental finding. look for vocal cord paralysis. esophagus. foramen of Bochdalex (3-5%. If the patient has a clinically suspicious lump. 32) If a patient with lung cancer presents with hoarseness. cheaper. anus). DO NOT DISTRIBUTE -5- . 31) In high-risk patients. the TIBC is often increased. 39) In resistant hypertension. fragmentation hemolysis. whereas anemia of chronic disease is marked by an unusually low TIBC. perhaps the most spectacular of the fragmentation syndromes. Some patients with acute lymphoblastic leukemia (ALL) also have 9:22 translocations (poor prognostic marker). 26) Patients with hereditary nonpolyposis colorectal cancer syndrome have a higher-than-average risk of developing colon and gastric cancer. seizures. consider and rule out renovascular hypertension. or esophagus). 36) The presence of bilateral small kidneys in a patient with azotemia confirms chronic renal failure. look for a squamous cell cancer (lung. 41) The principal mechanism of bicarbonate reabsorption in the proximal tubule is through Na+-H+ exchanger (NHE3) activity. 30) In a patient who has a malignancy involving the right hilum. 25) Regardless of what is done. cervix. but the problem is less frequent and smaller in magnitude with ARBs because of their less pronounced effects on aldosterone levels. and severe renal potassium wasting. chronic end-organ damage. Because up to 50% of patients develop gallbladder carcinoma. 49) The triad of thrombocytopenia. and hyposplenism. more common in women who have gallstones. usually left-sided). head and neck. 44) Bartter's syndrome is a disorder associated with normotensive hyperaldosteronism. in which portions of the long arms of chromosomes 9 and 22 are exchanged. It is thought that the cola acidifies the gastric contents and liberates carbon dioxide in the stomach. the presence of concomitant retinal disease suggests strongly (90% correlation) that the renal manifestations are due to diabetes. 40) New onset of nephrotic proteinuria in an elderly patient warrants exclusion of an underlying malignancy. 47) Both iron-deficiency anemia and anemia of chronic disease have a low transferrin saturation. look at the hand veins. and often by itself effective therapy. 35) Up to 15% of breast cancers may not be detectable by mammogram. 48) The main clinical manifestations of sickle hemoglobinopathies are hemolytic anemia. neurotoxicity in the form of ataxia. periodic vaso-occlusive disease ("crises"). 37) In a diabetic patient with proteinuria. 34) If a patient presents with hypercalcemia. 29) The three major openings in the diaphragm through which hernias may occur are the esophageal hiatus (most common). and episodic encephalopathy in patients with short bowel syndrome. 28) In patients with suspected perforation. resulting in the disintegration of phytobezoars. but less than 10% of all patients with ulcerative colitis have primary sclerosing cholangitis. 24) Three liters of Coca-Cola administered via nasogastric lavage over a 12-hour period can dissolve gastric bezoars.

a large cell with two nuclei. 61) Antinuclear antibody (ANA) titers are not associated with activity of disease. and syncope. vomiting. 78) The most common cause of dizziness is benign paroxysmal positional vertigo. nausea. HIV treatment guidelines change frequently . urticaria or angioedema. 55) Assuming that you are at sea level and breathing room air. a pleural malignancy associated with asbestosis exposure.30 suggest rheumatoid effusion. Decongestion with topical adrenergic agents may be needed initially to allow corticosteroids access to the deeper nasal mucosa. TB. sense of foreboding. lupus. 60) Early. 59) Mesothelioma. bronchospasm. prolong its cardiovascular and pulmonary manifestations. lymphoma. thrombocytopenia. 71) HIV infection is preventable and treatable but never curable. 64) Always check for Sjögren's antibodies (SSA/SSB) and phospholipid antibodies in a young woman with lupus before conception. 54) Any condition that leads to V/Q mismatching can cause hypoxemia. malignancy). a family history of thrombosis. and phospholipid antibodies can significantly increase the risk for miscarriage. 83) Elective surgery should be postponed for further evaluation if the patient has signs or symptoms of unstable or inadequately treated chronic disease. 74) A person under care for HIV should not develop pneumocyotic pneumonia (PCP). 79) The leading causes of death after a stroke are medical complications. premature labor. reflecting the distribution of these receptors in the skin. 73) Adherence to anti-HIV therapy must be > 95% for a durable response. not the stroke itself. or intrauterine growth delay. 72) If you are thinking of mononucleosis as a diagnosis. 62) COX2 NSAIDs are no more efficacious than older standard NSAIDs but are significantly less toxic. which can produce a low-grade synovitis and cryoglobulins (which in turn can produce a falsely positive RF). DO NOT DISTRIBUTE -6- . 57) Incidence of lung cancer now exceeds breast cancer in women. 56) Although the anterior segment of the upper lobes may be affected by TB. 75) There is a critical interaction between HIV and tuberculosis. 81) The sudden onset of a severe headache may indicate an intracranial hemorrhage. 76) If you have diagnosed one sexually transmitted disease (STD).always verify your information. 69) Chronic urticaria may require treatment with a combination of both H1 and H2 antihistamines. Work-up for an allergic etiology is rarely informative. 63) A patient with low positive rheumatoid factor (RF) and arthralgia should be checked for hepatitis C. pruritus. a lesion found only in the anterior segment suggests a diagnosis other than TB (e. hypotension. aggressive intervention with disease-modifying antirheumatic drugs reduces the morbidity (deformity leading to reduced functionality and disability) and mortality associated with rheumatoid arthritis. an easy way to calculate the A-a difference is as follows: (150-40/0. heart block). or malignancy.8) . 52) Secondary monoclonal gammopathy must be distinguished from the monoclonal gammopathy associated with multiple myeloma. abdominal pain. thrombosis at unusual sites (such as the mesenteric vein). solitary plasmacytoma. think about and test for HIV. and greatly decrease the effectiveness of epinephrine and albuterol in reversing the life-threatening manifestations of anaphylaxis.PaO2 measured by ABG.. diarrhea. not neurologic ones. This is the most common cause of hypoxemia and is responsive to oxygen therapy. 68) ACE inhibitors are often-forgotten causes of angioedema and chronic cough. 67) The clinical manifestations of anaphylaxis include flushing. 66) Intranasal steroids are the single most effective drug for treatment of allergic rhinitis. It is entirely preventable. or recurrent thrombosis without precipitating factors suggests a hypercoagulable state. 82) Coma is usually caused by medical problems. you must consider others. 53) Deep venous thrombosis in a young person. If one infection is present. headache.g. Most pulmonary disorders are associated with some degree of V/Q mismatching. Women develop lung cancer at an earlier age and after fewer years of smoking. 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. Sjögren's antibodies increase the risk of neonatal lupus (rash. 77) Most back pain is not caused by a radiculopathy. and Waldenström's macroglobulinemia. each possessing a distinct nucleolus. amyloidosis. tachycardia. 58) Pleural fluid glucose < 30 mg/dL and pH < 7. especially HIV. hoarseness. look for the other. is not associated with tobacco use. 70) Beta blockers should be avoided whenever possible in patients with asthma because they may accentuate the severity of anaphylaxis.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. stridor. benign monoclonal gammopathy of uncertain significance. 80) Heparin has no value in the acute treatment of strokes.

or lithotripsy. 90) Influenza virus vaccination reduces hospitalization and death from influenza and its complications in elderly and high-risk patients. If the compression is caught early enough when the patient is able to ambulate. urinary retention. the Geriatric Depression Scale. MD -------------------------------------------------------------------------------------------------------------------------------------------Spinal Cord Compression * A 61yo AAM is brought to the ED complaining of back pain that started gradually three days ago. positive Babinski sign. increased tone.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. If we’re suspecting spinal cord compression. not MRI of the spine. bilateral lower extremity weakness. * 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. -------------------------------------------------------------------------------------------------------------------------------------------Kaplan Videos (2001) – Neurology with Dr. not bone scan. as distinct from systolic dysfunction. 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. 98) Delirium carries tremendous mortality and morbidity rates and should be identified. thromboembolism. * The prostate cancer is important because metastatic disease to the spine could be compressing the spinal cord. It is essential to ask about falls. and treated as any medical emergency. First thing to think about is if this is an emergency or not an emergency. looking for ulcerations. even if the patient has received prophylaxis. their ability to ambulate after proper treatment is about 80%. worked up aggressively. Next step in the management of this patient is give dexamethasone. His past medical history is significant for prostate cancer diagnosed three years ago. lymphoma. stroke. 87) Pacemakers and implanted cardioverters/defibrillators should be assessed both before and after surgery. 92) Closely monitor patients with blood pressure measurements defined as "prehypertension. 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. 96) Commonly used instruments for a comprehensive geriatric assessment include the Mini Mental State Exam. meaning do we need to intervene right now or can we treat with something like analgesics and follow-up. lung. 85) Acute dyspnea in a patient who has had major surgery should raise the suspicion of pulmonary embolism. given the significant mortality and morbidity of hip fractures. and then act accordingly. and breast cancer before prescribing estrogen/progesterone therapy in menopause. and medications to treat osteoporosis. 89) Strict bed rest is not needed for the treatment of acute lumbosacral strain. 97) Dementia and short-term memory loss are not caused by aging. we should see upper motor neuron lesion signs below the level of the compression. fecal incontinence.g. 99) Diastolic dysfunction. radiation therapy. instrumental activities of daily living. So just the history of cancer with back pain means we should be evaluating this acutely. urinary incontinence. or reduced blood flow. Consider therapy before diagnostics in management DO NOT DISTRIBUTE -7- . 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. 93) Reduce the risk of hip fracture in elderly and high-risk patients with calcium and vitamin D supplements. when indicated. spastic paralysis. exercise prescription. activities of daily living. He describes the pain as band-like around the abdomen without radiation. assess for fall risk. * Most likely diagnosis is spinal cord compression. not x-ray. Jacob Levy.a trend that is expected to continue for the foreseeable future. and assessment of stability and mobility (e. sexual dysfunction in males. 100) Fifteen percent of elderly patients who fall and fracture a hip report prior falls. Signs would include hyperreflexia. 95) Older adults currently constitute the fastest-growing population in the United States . Although the symptoms of diastolic and systolic dysfunction may be similar. Other worrisome signs with back pain would be fever. multiple myeloma. injury.. Tinnetti or "Get Up and Go" test). 94) Assess a woman's risk of coronary disease. Other worrisome cancers could be breast. hip pads." and encourage lifestyle changes to prevent progression to hypertension. 91) Always examine the feet and pedal pulses of diabetic patients regularly. 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.

blurry vision. * Focal neurologic deficit of sudden onset is very likely to be a stroke. breathing. unable to understand. Broca is broken speech. obesity. Pathophysiology is lack of blood supply to section of the brain. Broca aphasia is expressive aphasia with intact understanding. circulation. sensitive maybe 80% of the time. diabetes. Could be an embolus coming from the atrium in a patient with atrial fibrillation. * Patient presents with signs of cord compression. where the clot forms in the brain itself (not an embolus from a distant site). then do radiation. hypertension. complaining of sudden onset of right upper extremity weakness that started while she was watching television in the morning. (sensory) pain/temperature lost on lower extremities. Most sensitive test is an MRI. * Patients with MCA infarcts present with contralateral hemiparesis involving the face and the arm more extensively than the lower extremity. “little man on your brain. It could be a bleed in a patient with hypertension. usually with ataxia and pyramidal signs like hyperreflexia and positive Babinski. first initial step is give dexamethasone. and light touch intact. (CN) cranial nerves intact. So. If there is an anatomic problem in the spinal cord. HIV. and the presence of intact proprioception/vibration sense. Characteristic signs of vitamin B12 deficiency are loss or proprioception and vibration with intact pain/temperature. dysphagia. Aphasia occurs with dominant hemisphere stroke. -------------------------------------------------------------------------------------------------------------------------------------------Cerebrovascular Accidents (CVA) * 56yo woman is brought to the ED by her daughter. So he puts is feet up and lays back. * Most likely diagnosis is syringomyelia. * Risk factors for cerebrovascular disease are the same as coronary artery disease. It could also be thrombosis. and alcohol abuse. You perform a thorough neurological exam. -------------------------------------------------------------------------------------------------------------------------------------------Syringomyelia. even if they’re showing you MRI. Anterior is the middle cerebral artery (MCA) and anterior cerebral artery (ACA). * Radiation therapy and surgical decompression are generally left for after the diagnosis is made. male gender. So. Vitamin B12 Deficiency & Anterior Spinal Artery Infarction * A 25yo man comes to the Emergency Department status post motor vehicle accident. patient could have sudden onset of diplopia. Best initial test is x-ray. nonsensical speech. pons. * Best initial test for syringomyelia is an MRI. Say it is lymphoma or cancer compressing the spinal cord. while vibration/position and light touch are in posterior column. Her daughter became concerned when her mother was unable to talk in response to her questions. finding (motor) lower extremity weakness 4/5 bilaterally with some hyperreflexia. On neurologic exam. Posterior is vertebral arteries forming the basilar artery and the posterior cerebral artery (PCA). Best initial test is a spinal x-ray. General atherosclerosis risk factors include smoking. So an anterior spinal artery infarct would have lost pain/temperature sense. An MRI shows osteomyelitis compressing the anterior cord. * Important risk factors include atrial fibrillation. ACA ischemia may involve urinary incontinence and personality changes (Phineas Gage).Study Notes – Internal Medicine James Lamberg 28Jul2010 when the patient has an emergency. Most accurate test is MRI of the spine. * Basilar artery provides blood supply to cerebellum. then do surgical decompression. such as in a watershed infarct. Treatment is often surgical. Most people are left-hemisphere dominant. Wernicke aphasia is wordy. * There is an anterior circulation and a posterior circulation to the brain. vibration/position intact. and calls you to evaluate the patient. and brainstem. with a pool of fluid developing in the spinal cord.” has to sleep comfortably at night. focal cranial DO NOT DISTRIBUTE -8- . peripheral vascular disease. Mnemonic is “put your best foot forward” for foot/leg affected with forward/anterior artery. valvular disease (especially mitral stenosis). Say you gave dexamethasone and diagnosed. When you question the patient. she seems to understand what is being said but she cannot clearly respond. The ED physician has addressed the airway. * Homunculus. now there is an abscess or hematoma compressing the spinal cord. recent transient ischemic attack (TIA) with similar symptoms. Pain and temperature lost because these spinal cord tracts are centrally located (spinothalamic). there should be an anatomic solution. sudden onset of flaccid paresis. high cholesterol. * Patients with ACA infarcts presents with contralateral hemiparesis involving the leg more than the face/arm. * Vitamin B12 deficiency causes subacute combined degeneration of the cord. * MCA infarct also comes with aphasia. increased age. Best test is MRI. you note right upper extremity weakness with pronator drift and right facial palsy. or carotid artery disease. Anterior circulation on interior (leg) and middle circulation on outside (arm/face). * Most likely diagnosis is cerebrovascular accident (CVA). * Anterior spinal artery feeds the sensory neurons involved in pain and temperature. Brainstem (medulla/pons/midbrain) is where cranial nerves are. Hypotension can also induce ischemia. patient would have facial droop and weak upper extremity.

* Must document time of onset and CT scan with diagnosis before giving tPA. add dipyridamole. or stroke in evolution.000. On neurologic exam. and symptom onset is within 3 hours. giving us the ability to see. * What is the most likely diagnosis? Answer is seizure. not heparin. * With ischemic stroke. * Hemorrhagic stroke is managed by supportive care and consulting neurosurgery (poor prognosis). If you give tPA past the 3-hour window. * If patient was sleeping and woke up with symptoms. Answer is not surgery. not aspirin. atrial fibrillation (24h Holter monitor). urinary tract bleed) within past 21 days. If there is no bleeding on the non-contrast CT. Clopidogrel side effects include TTP and neutropenia. bleed). Cerebellar signs include ataxia and vertigo. 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. * Stoke in evolution is when symptoms are getting worse. but we give it anyway. GI bleed. * If the patient is allergic to aspirin. * PCA supplies occipital lobe. * Heparin reduces the rate of recurrent CVA. * Ticlopidine is never the answer due to side effect. or is allergic to clopidogrel. ischemic stroke or head trauma within 3 months. do we give contrast or no contrast? We are trying to distinguish between a bleed and ischemia. * Contraindications for tPA therapy are bleeding (e. failed aspirin therapy. ticlopidine.g. Symptoms mean you have to be able to blame a TIA or a stroke on the stenosis. we can think about giving aspirin. a loss of brain function occurs with brain cell death. PT > 15sec. basilar artery thrombosis. CT shows no bleeding. * 56yo woman is brought to the ED by her daughter. So the risk to benefit ratio is not favorable after 3 hours. Indication for carotid endarterectomy (CEA) is >70% stenosis with symptoms. tPA should not be given even if you get the CT minutes later. then answer is tPA/PLAT (tissue plasminogen activator). Carotid duplex finds 80% stenosis of the right internal carotid artery. When you question the patient. Her daughter became concerned when her mother was unable to talk in response to her questions. Most likely diagnosis is MCA infarct (left side). which are TTP and neutropenia. For every stroke you prevent. * A cranial nerve III deficit (cannot adduct eye) on one side and hemiparesis on the other is Weber syndrome. We are looking for the absence of blood. Now. you cause one complication (e. not transthoracic echo. There is a higher risk of recurrent CVA if the patient has ischemic stroke with atrial fibrillation. you are sure it is ischemic stroke. For ischemic stroke. * Clopidogrel is used if the patient has failed aspirin therapy. you’re looking for the presence of white material in the parenchyma of the brain. * With posterior circulation (basilar artery). In ischemic stroke. because these two have different management. the stenosis would be on the left side (not the right). say due to arrhythmia. visual loss. neutropenia) more often. clopidogrel. -------------------------------------------------------------------------------------------------------------------------------------------Seizures * 29yo man is brought to the ED by ambulance after his mother found him convulsing in his bedroom. we assume ischemic stroke. meaning the patient is on aspirin after an ischemic stroke then has another ischemic stroke. look for reversible risk factors such as cardiac thrombosis (echocardiogram). * Say you do a workup on the 56yo lady that has right-sided facial/arm hemiparesis. ataxia) on the opposite side. A cross syndrome is a cranial nerve deficit on one side. MRI most sensitive for posterior fossa lesions. * If patient has acute onset focal neurologic deficit. * Patient has arm/face hemiparesis and Broca aphasia. tPA. DO NOT DISTRIBUTE -9- . So the only time you give heparin is when you have a higher risk of CVA. Next step in management is head CT scan. complaining of sudden onset of right upper extremity weakness that started while she was watching television in the morning. and a motor deficit (hemiparesis. * When looking at a CT scan to evaluate a suspected CVA. Differentiate seizure from syncope. She then called the ambulance to bring her son to the hospital. BP > 185/110. If the patient’s symptoms were due to the carotid artery stenosis. not ticlopidine. Cross syndrome is most likely posterior circulation stroke. PCA ischemia comes with hallucinations. The difference between clopidogrel and ticlopidine is that ticlopidine causes the side effects (TTP. you’re only increasing their risk of bleeding. not clopidogrel. you note right upper extremity weakness with pronator drift and right facial palsy. * A sensory loss on one side of the face with contralateral sensory loss on the body is Wallenberg syndrome. she seems to understand what is being said but she cannot clearly respond.Study Notes – Internal Medicine James Lamberg 28Jul2010 nerve palsies. platelet count < 100. The benefit of aspirin in acute stroke is not as good as with acute myocardial infarction. * Aspirin is used in ischemic stroke for secondary prevention. not transesophageal echo. mainly for anterior circulation stroke). not tPA. surgery within past 14 days. intracranial bleed ever in the past. CT scan without IV contrast is most sensitive test for hemorrhagic stroke.g. Answer is head CT without contrast. The mother says he was tired and lethargic for 20 minutes after the episode. * A cranial nerve III deficit on one side and ataxia on the other is Benedikt syndrome. the tissue will look darker than the surrounding tissue. heparin. * Most sensitive (accurate) test for diagnosing ischemic stroke is MRI. deficit is contralateral if above decussation and ipsilateral if below. carotid artery stenosis (carotid artery duplex.

this is status epilepticus. generalized. Then what do you give? Answer is phenytoin or fosphenytoin. If the patient has positive family history. negative family history. The most specific thing on history for seizure is the post-ictal state. * Urinary and bowel incontinence plus bite marks are seen more commonly in seizure than syncope. treat it. the patient was tired/achy for 20minutes. Ask if the patient has a history of epilepsy. We follow the patient. A generalized seizure affects the entire cortex. Either the seizure starts as generalized. What is the best initial treatment now? Answer is give lorazepam or diazepam. Once the patient has another seizure. breathing. but not necessarily specific. * If patient is continuing to seize without regaining consciousness between. * The next step in management is ABCs: airway. as it is the most widely effective seizure medication. A seizure is considered a complaint. simple. * What if patient continues to seize after giving phenytoin or fosphenytoin? Give phenobarbital. * 29yo man comes in with new-onset seizure witnessed by his mother. and the patient is already intubated. so patient has “drop attacks. * Medication for generalized seizure is valproic acid or lamotrigine. Suspect infection if the patient has seizure with fever. SLE stigmata. So this is the clear differentiation. * Seizures are categorized into partial. * So patient has normal neurologic exam. pick valproic acid. or the foot. bleed. high sodium. So patient might have shaking/jerking of the hand. so patient keeps postural tone but brain shuts down so the patient is not paying attention (no consciousness) and likely just blinking. and circulation. low magnesium. * Seizure differential mnemonic: VITAMINS.” An absence seizure is the opposite of an atonic seizure. DO NOT DISTRIBUTE . * Medication for partial seizure (even one that becomes generalized) is carbamazepine or phenytoin. For metabolic. or with achy muscles. tired. Here. arthritis. or photophobia. neoplastic (metastatic cancer. like a patient coming in with chest pain. Note. low glucose. Syncope has rapid recovery within minutes or seconds after unconsciousness. low oxygen. An atonic seizure means lack of tone. negative EEG. Patients who syncopize can have tonic/clonic movements. or nuchal rigidity. hoping seizures resolve. and complex vs. If carbamazepine or phenytoin are not answers. look for risk factors and sudden onset of neurologic focality. Management is lorazepam or diazepam. infection (encephalitis. for acutely seizing patient. Blood pressure and circulation are intact. drugs). there is a large differential diagnosis for seizure. Bite marks on the tongue may imply seizure. * Medication for unidentifiable seizure is valproic acid. A complex partial seizure is treated differently from a complex generalized seizure. * Medication for absence seizure is ethosuximide. metabolic (electrolytes. autoimmune (vasculitis. lorazepam/diazepam. or the leg. phenobarbital. treatment would be focused on hypertonic saline. * Say you give the benzo and the patient is still seizing. AVM). * Always look for a secondary cause. think about metastatic to the brain. * What if EEG is negative. purpura. or a partial seizure turns into a generalized seizure. Patients who have syncope and come out will not be lethargic. when do you start treating an idiopathic seizure? Answer is with recurrent seizures. * A partial seizure only affects one part of the brain. If you identify a secondary cause. low-grade fever with weight loss. we start treatment. Suspect autoimmune if history involves a rash. A complex seizure implies loss of consciousness. positive ANA. primary tumors). If a young woman with breast cancer has a seizure. trauma. the post-ictal state still is the most specific symptom. low calcium. idiopathic. glucose.10 - . Then benzodiazepine. convulsing with a long post-ictal state. A simple seizure has no loss of consciousness. SLE).Study Notes – Internal Medicine James Lamberg 28Jul2010 This patient was having convulsions (tonic-clonic movements). and one seizure. giving phenytoin IV is not recommended due to lack of solubility and resultant precipitation. s for Psi or psychiatric (patient faking). So patient has first time seizure with no exact etiology. * If you’re thinking vascular disease. Categories help determine what medication to give. Patient is continuing to seize. but not specific either. * Ask yourself if there is an underlying cause for the seizure. meningitis). treatment would be focused on intubation and high-flow oxygen (after ABCs). * What is the best test to identify abnormal neural activity that predisposes to a seizure? Answer is electroencephalogram (EEG). Myoclonic seizures involve muscle jerks. Do not assume that any seizing patient has a diagnosis of epilepsy. we would start right away at the first seizure. order an EEG. Urinary or bower incontinence is an important part of the history. * A seizure is defined as random firing of neurons in the brain. So if patient comes in seizing with sodium of 106. phenytoin/fosphenytoin. look at things like low sodium. give fosphenytoin instead. * Seizure Meds: ABC. and last midazolam/propofol. However. * Medication for atonic or myoclonic seizure is valproic acid. If patient came in hypoxemic and seizing. * Next step after phenobarbital? Answer is midazolam and propofol (anesthesia). * Seizure: vascular (stroke.

manganese. When questioned. what is the most likely diagnosis? Answer is Parkinson disease. * Side effects are psychosis. and there are no other stigmata of cerebellar or Parkinson disease. paucity of movement). the most effective treatment for Parkinson disease. and ropinirole. Carbidopa inhibits the conversion of levodopa to dopamine in the periphery. the tremor occurs and worsens with movement. COMT inhibitors. which are dopamine antagonists. tumor. Response fluctuations are the “on/off phenomenon. After long-term therapy on carbidopa/levodopa.g. there is a family history usually. * So in the 56yo man with resting tremor. With postural instability. In cerebellar disease. * Answer dopamine agonists (e. Acetylcholine acts to inhibit dopaminergic tone in the brain. and cogwheel rigidity (arm feels like cogs on a wheel. trihexyphenidyl). On/off phenomenon is quite distressing to patients. like ropinirole (not selegiline or COMT inhibitor). MPTP: an unintentional byproduct of the recreational drug MPPP). -------------------------------------------------------------------------------------------------------------------------------------------Huntington Disease * 34yo man comes to your clinic for evaluation of strange spontaneous movements that have been occurring lately. pramipexole. * Normally when you walk and turn it is a smooth movement. dry eyes. and cerebellar disease. the tremor occurs at rest and resolves with movement. add the dopamine agonist. the tremor occurs primarily with movement (intention tremor).11 - . So treatment is to either give dopamine to provide what is lost. In essential tremor. Know that patients will present with abnormal movement (chorea). DO NOT DISTRIBUTE . how do they function on a day-by-day basis? * Functional patients get amantadine or anticholinergic (e. essential tremor. patients get response fluctuations. So ask yourself about secondary causes. more so than younger patients. * If patient is on carbidopa/levodopa and it isn’t enough. We don’t give carbidopa/levodopa to functional patients because it has the most serious side effects. and when walking the patient is stooped forward making small steps.” akinesia (restlessness). patient turns in wide circle. diagnosis of Parkinsonism is clinical. You can also give a COMT inhibitor or selegiline. His family history is significant for his father who died at age 41 of dementia. * The most preferred dopamine agonists are the newer ones. You can decrease the amount of dopamine by antagonizing it (decreasing it directly) or by increasing acetylcholine. * Say patient is functional and just has a tremor. so that the levodopa can reach the brain and be converted to dopamine there. Physical exam finds a resting tremor noted in his right hand. moving in distinct steps). pramipexole. the patient experienced uncontrolled grimacing with grunting. You note cogwheel rigidity in his right upper extremity with a positive Myerson sign (patient unable to resist blinking with glabellar tapping). cobalt. * Most likely diagnosis is Huntington disease. * Causes of Parkinsonism are drugs (antipsychotics. * Parkinsonism is defined as death of dopaminergic cells in the substantia nigra. dry mouth. In Parkinson disease. * Selegiline (MAO-B inhibitor). * Dopamine agonists are bromocriptine. Is this patient diabetic and taking metoclopramide for autonomic neuropathy with gastric paresis? * Most cases of Parkinson disease are idiopathic. meaning we cannot identify a cause. thus we can give less levodopa and get the same effect. and amantadine increase dopamine amount/effect also. His past medical history is significant for mild hypertension treated with a thiazide diuretic. pergolide.g. and dyskinesia (abnormal movements). Exam for cerebellar disease would include finger-to-nose and heel-to-shin tests. bleed or stroke. the patient will have pillrolling tremor at rest. with the patient have a compromised ability to reach the object. * Differential diagnosis for tremor includes Parkinson disease. * Non-functional patients get carbidopa/levodopa. So. She also states that her husband has been moving very slowly as of late. We avoid anticholinergic medications in elderly patients because they can become confused. pick amantadine if patient is > 65yo. In Parkinson disease. CO poisoning. history of falls (postural instability). the answer is selegiline. and acute GI upset. Recently while sitting at a family dinner. slow movement (bradykinesia. metoclopramide. carbidopa/levodopa. Pick trihexyphenidyl if patient is < 60yo. or to take away acetylcholine so the dopamine in the brain can work more effectively. hypotension. * The drugs that cause Parkinson are antipsychotics. the patient states that he feels fine and does not know why his wife is dragging him from doctor to doctor.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. * Acetylcholine blocking with trihexyphenidyl primarily. * 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. have urinary retention. * Say patient has stigmata of Parkinson and you are asked what medication is thought to arrest the progression of Parkinson disease. * Always ask how much function you are getting from the treatment at the expense of the side effects. ropinirole) to treat response fluctuations for patients that are taking carbidopa/levodopa.

changes in personality. not lumbar puncture. multi-infarct dementia (stepwise progression. -------------------------------------------------------------------------------------------------------------------------------------------Dementia * A 67yo woman is brought to your clinic complaining of forgetfulness. HIV. * Medications useful to arrest the progression of MS are interferon beta 1a. coronary artery disease. * Treatment for acute exacerbation of MS is IV high-dose steroids with a 4-week taper on oral prednisone. difficult to differentiate from Alzheimer). * Treatment for fatigue in MS is amantadine. * Treatment for urinary incontinence in MS is oxybutynin. * Most common cause of dementia is Alzheimer disease. violence. least common. there is initial memory loss that becomes chronic and gradual with relative preservation of social function and personality until late in the disease. * Testing includes MRI with gadolinium. * Pick disease (frontal lobe degeneration) has personality changes initially. Looking for multiple lesions and paraventricular lesions consistent with MS. No medication has been shown to help with primary progressive disease. * The best initial test is also MRI. and a family history of a similar thing happening to a first-degree relative (Huntington is autosomal dominant). frontal lobe neoplasm and chronic subdural hematoma (check for focality on exam or trauma history). waxing/waning). uremia and cirrhosis (check creatinine. interferon beta 1b. CVA. syphilis (check RPR: rapid plasma reagin). * With memory loss. central or obstructive sleep apnea (look for obesity. * Treatment for spasticity in MS is baclofen. she states that three years ago she had an episode of seeing double that lasted two days that resolved on its own. Lewy body disease (delirium-like course. * The essential point for clinically suspecting MS is a patient with multiple neurologic deficits that are separated by space (anatomically) and by time (temporally). * Relapsing/remitting disease is a form of MS where patient goes through waxing/waning episodes of symptoms.12 - . * Brain tumor less likely as there is no specific tumor location giving lower extremity weakness along with diplopia. but not in primary progression. * Clinical diagnosis is presence of chorea with personality changes. 85-95% sensitive. None of these three is better than the other. consider dementia and ask yourself if there is a reversible cause. * Relapsing/remitting disease can become progressive (secondary progression). * CVA less likely because she is 32yo with no other listed risk factors. but they help symptomatically for the disease relapse. looking for chromosome 4p CAG repeat. or glatiramer acetate. * Cervical spinal disease or carpal tunnel less likely because they do not explain the diplopia. cervical spinal disease. She states that her symptoms began several days before admission and have progressively worsened over the last several hours. * Olfactory/visual evoked potentials are not used much today with the development of MRI. there is no formal treatment. 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. * Reversible causes: hypothyroidism (check TSH). True diagnosis done with genetic analysis. and worse prognosis. loss of inhibition. In Alzheimer disease. When asked.Study Notes – Internal Medicine James Lamberg 28Jul2010 abnormal behavior. * Non-reversible causes: Creutzfeldt-Jakob disease and prion disease (check for myoclonus. speak with spouse). LFTs. DO NOT DISTRIBUTE . CSF for oligoclonal banding. Primary progressive disease has worsening MS symptoms right from presentation. Steroids do not slow down the progression of the disease. They have been shown to help with relapsing/remitting forms. * Differential includes MS. Physical exam is unremarkable. -------------------------------------------------------------------------------------------------------------------------------------------Multiple Sclerosis (MS) * A 32yo woman comes to the ED with numbness and tingling in her right hand. * Most likely diagnosis is multiple sclerosis (MS). Her past medical history is significant for hypertension. rapid dementia course usually weeks to months). and olfactory/visual evoked potentials looking for abnormal transmission. physical exam). Physical exam is significant for hyperreactive reflexes bilaterally in the lower extremities. * If MRI is inconclusive or equivocal for the clinically suspected MS diagnosis. You also note increased spasticity in her lower extremities. * What is the most sensitive/accurate test? Answer is MRI or brain and spine. such as agitation. brain tumor. * Treatment for urinary retention in MS is bethanecol. usually in a patient 30-40yo with a positive family history. vitamin B12 deficiency (check B12 level). and high cholesterol. * Treatment is supportive care. then get the lumbar puncture. and carpal tunnel syndrome. tie temporally dementia onset with CVA. not CT scan.

Treatment of choice is diuretics. * Ménière disease is a triad of (peripheral) vertigo. Treatment is meclizine (antihistamine) or diazepam in severe cases. nystagmus non-suppressible with fixation. and tension. The patient describes walking to her bathroom and experiencing a sudden feeling of nausea. 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. like they are falling forward. MS. tinnitus. The headache is worsened by walking up stairs or around the block. or executive function. e. give meclizine initially then diazepam secondary. * Treatment for Alzheimer disease was tacrine. Most likely diagnosis is a migraine. -------------------------------------------------------------------------------------------------------------------------------------------Headache * A 32yo woman comes into the office complaining of a headache that started two days ago. 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. do MRI imaging of the posterior fossa. * If you cannot identify a disease. symptoms aggravated by cough. we do MRI. A trigger is very specific for migraine. hearing loss. * Medication of choice for Alzheimer now is donepezil. She locates her headache to the right side of her head and describes it as pulsating and throbbing in quality. progressively worsening headache. * Central vertigo is usually chronic. cluster. headache occurs after vomiting. “worst headache of my life” (subarachnoid). chest pain. * Vertigo is the sensation of movement in the absence of movement. or labyrinthitis with their treatments listed. * Primary headache disorders include migraine. Patient may say I move my head then 5-10 seconds later I get dizzy. focality on CNS exam. Physical exam can reproduce symptoms via Dix-Hallpike test (head movement testing). shortness of breath. uni-directional nystagmus * Posterior fossa imaged more effectively with MRI than with CT scan. and tinnitus unrelated to head movement. Then rule out non-reversible causes like Pick (personality changes first). nystagmus suppresses with fixation. * Ask yourself. Disease is thought to be caused by swelling in the semicircular canals. BPPV. * Migraines are associated with triggers. we diagnose Alzheimer disease. * Benign positional paroxysmal vertigo (BPPV) is peripheral vertigo of sudden onset related to movement of the head. Then rule out or treat reversible causes. Perform MMSE to find dementia. nuchal rigidity. there is no focality on physical exam. hearing loss. thunderclap headache (time to peak pain was seconds). such as eating a specific food (e. Treatment of choice is movement exercises to try and move the otolith out of the canal. and surgical decompression if medical management fails. If you identify peripheral vertigo. On exam. “Dizzy” is very nonspecific and does not have much significance medically. she has had these headaches a few times before. fever. such as concentration. Do not pick tacrine for first line. stress. multi-directional nystagmus * Peripheral vertigo is usually acute. praxis. * Labyrinthitis is peripheral vertigo that occurs when vertigo follows an upper respiratory tract infection. Now. She also states that loud noise and bright light exacerbate her pain.g. if you find central vertigo signs on physical exam. and Lewy body (delirium-like). pure nystagmus (in one direction. chocolate). we do symptomatic treatment. usually vertical). * Patient presents with memory loss. She describes the feeling of the room spinning around her even though she realizes she is not moving. For central. worse in the early morning. She admits to nausea but denies vomiting. multiinfarct dementia (temporal tie to CVA). sleeping too little.13 - . any headache starting at age > 55yo. mixed nystagmus (usually horizontal but with another component). or during menstruation. the earth is rolling in front of my feet. She managed to reach the bathroom where she vomited once and fell to the floor a second time. DO NOT DISTRIBUTE . She was unable to get up off the floor and called 911. * Differentiating between vertigo and pre-syncope is a clinical determination.g.Study Notes – Internal Medicine James Lamberg 28Jul2010 * Dementia is generally memory loss plus some other deficit in cognitive function. posterior fossa tumor. light headed. medication) or peripheral (ear semicircular cannals). -------------------------------------------------------------------------------------------------------------------------------------------Vertigo * A 53yo woman is brought to the ED complaining of dizziness. palpitations. rapid progression). Etiology is thought to be an otolith in the semicircular canals. neighborhood signs (cranial nerve deficits via brainstem). low salt diet. CJD (myoclonus. for peripheral. * Next question after determining vertigo is if it is central (in the CNS. * So. This implies cardiac disease. but no longer used as the drug of choice due to liver toxicity. seek Meniere. This is where the mini-mental status exam (MMSE) is important. Patient may say the room is spinning around me. * Most important question is to identify what the patient means by dizziness. aggravated by valsalva maneuver.

like acetaminophen or NSAIDs. especially in the muscles of the throat and eyes (dysphagia. looking at CSF for high protein that is not accompanied by pleocytosis (a high number of cells). IVIG and plasmapheresis are equivalent in their effect. Approximately three weeks ago the patient states that he experienced several episodes of diarrhea that resolved spontaneously. * The best test (most accurate) for GBS is an electromyogram (EMG). * Management for mild migraine headache (no nausea or vomiting). * Photophobia and phonophobia (ligyrophobia) classically occurs in migraine but may occur in cluster also. * Best initial treatment for GBS is intravenous immunoglobulin. * The best initial test for the diagnosis of GBS is lumbar puncture. you just gave them an MI. In the context of clinical suspicion of myasthenia. CIDP (chronic) has a slower course. Migraines are generally caused by vasodilation and sumatriptan constricts the vessels. Prophylaxis for migraines is indicated when patient has more than 3 headaches per month. * Campylobacter jejuni infection (gastroenteritis) associated with Guillain-Barré syndrome (GBS). distribution starts in distal areas and moves proximal. has rhinorrhea. or verapamil. * The distribution of weakness is important when differentiating between Guillain-Barré. red eye. So if a patient has a 70% left main coronary lesion and you give them sumatriptan. there typically is not a distal to proximal movement. Do not give it even if you have high suspicion of CAD. sweating) are also seen. You can also do plasmapheresis. an AIDP. Cluster headaches peak usually within 5 minutes (quick onset) and only last 45-90 minutes. * Management for tension headache is analgesics. -------------------------------------------------------------------------------------------------------------------------------------------Myasthenia Gravis (MG) * A 35yo woman comes to the clinic complaining of double vision that seems worse near the end of the day. IV Ig is easier to give than arranging for plasmapheresis. Paresthesias (tingling) and autonomic instability (labile blood pressure. DO NOT DISTRIBUTE . * Only answer tensilon testing when there is no answer choice for acetylcholine receptor antibody. The patient states that his symptoms began two days ago. * A positive tensilon test is not specific for the diagnosis. * The best initial test for diagnosing myasthenia is serology for the anti-acetylcholine receptor antibody. Prophylaxis is propranolol. The patient also complains of difficulty chewing meat and other hard foods. Do not give prednisone or systemic steroids in the treatment of acute Guillain-Barré syndrome. occurring in clusters. no trigger. * Clusters happen 2-3 times per day over a 4-8 week period. the patient is noted to have bilaterally lower extremity weakness with loss of reflexes. are bilateral. Patients complain of easy fatigability. prednisone. * Migraines peak within 4-72 hours from onset of pain (gradual onset). anti-acetylcholine receptor antibody is extremely specific for the diagnosis. diplopia). * Cluster headaches are usually unilateral (like migraine).Study Notes – Internal Medicine James Lamberg 28Jul2010 * Pulsatile headaches occur in cluster and migraine headaches (both vascular). so IV Ig best initial treatment. You also note weakness of the upper extremities when the patient is asked to clench her fists around your fingers repeatedly. seen in HIV. ptosis. anhidrosis). * Hyporeflexia seen in any peripheral neuropathy. * Management for cluster headaches starts with 100% oxygen. On neurologic exam you notice snarling appearance when the patient is asked to smile and a nasal tone to her speech. * Most likely diagnosis is Guillain-Barré syndrome. possibly Horner syndrome (ptosis. A tensilon test is not the initial test. miosis. She notices that her symptoms improve following a good night sleep. and botulism. Lou Gehrig disease). or methysergide (generally not used because it causes retroperitoneal fibrosis). So you’re looking for high protein and few cells. If migraine is moderate to severe. On neurological exam. vice-like. * Tension headaches are triggered by stress but not foods or emotion. * Most likely diagnosis is myasthenia gravis (MG).14 - . Next line is sumatriptan. give NSAIDs. Prophylaxis for cluster headaches includes lithium. Symptoms are not acute either. timolol. * Never give sumatriptan to a patient with a history of coronary artery disease. In Guillain-Barré. myasthenia gravis (MG). false positives seen in other diseases like amyotrophic lateral sclerosis (ALS. * In MG. * MG is defined as muscle fatigue after repetitive motion of chronic onset with preferential involvement of the ocular and the pharyngeal muscles. radiating to neck or back of the head. -------------------------------------------------------------------------------------------------------------------------------------------Acute Inflammatory Demyelinating Polyradiculoneuropathy (AIDP) * A 46yo man is brought to your office complaining of rubbery legs. abortive therapy is sumatriptan or ergot alkaloid.

Study Notes – Internal Medicine

James Lamberg

28Jul2010

* 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.

DO NOT DISTRIBUTE

- 15 -

Study Notes – Internal Medicine

James Lamberg

28Jul2010

* 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.

DO NOT DISTRIBUTE

- 16 -

Study Notes – Internal Medicine

James Lamberg

28Jul2010

-------------------------------------------------------------------------------------------------------------------------------------------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.

DO NOT DISTRIBUTE

- 17 -

* On exam you find pulmonary hypertension. * No good treatment. want biopsy. all volumes are diminished. Postural therapy. * Unilateral hilar lymphadenopathy not seen in sarcoid. “ground glass” appearance. Could biopsy supraclavicular node if it is available. * Pneumoconiosis comes with opacities and irregular densities on CXR. In cystic fibrosis. and MCP joints. with well demarcated 3-4cm papules over the anterior aspects of the legs. Generally no lung involvement in Crohn disease. This is not a test of choice. PIP joints. -------------------------------------------------------------------------------------------------------------------------------------------Occupational Lung Disease * Typically occurs 10-20 years down the road. If no improvement. normal FEV1/FVC). and metastasis. What PFTs would you expect? Pattern is similar to restrictive. * Uveitis usually occurs rather abruptly. * Patients may have angiotensin converting enzyme (ACE) elevations.Study Notes – Internal Medicine James Lamberg 28Jul2010 * Be aggressive with pulmonary physical therapy. boilers. are ingested by macrophages. So either give steroids or refer immediately to the ophthalmologist for slit lamp exam. * All have a restrictive lung pattern so come with decreased PFTs. lead inhalation. temporal arteritis. pain in the eyes. not helping to brush out infection. Worry more about things like TB. * On chest x-ray with sarcoidosis. * In asbestosis there is a synergistic cancer effect with smoking. This is dextrocardia with situs inversus. She has no other complaints except joint swelling and pain that occurred three days ago. What is the next step in confirming diagnosis? * The painful red nodules on the shins are erythema nodosum. seen in older patient. not sensitive or very specific. -------------------------------------------------------------------------------------------------------------------------------------------Interstitial Fibrosis * Almost always idiopathic. and nasotracheal suction. * Pulmonary toilet (pulmonary hygiene) is helpful here too. shipyard workers. * These patients require the same vaccinations as in COPD. Also have immotile sperm. liver granulomas with elevated LFTs. so you expect a restrictive lung pattern (decreased PFTs. asbestosis. uveitis (ocular emergency requiring steroids). * Sarcoid more commonly seen in younger patients and in African American patients. and causes scaring over the years. pipes. copper. -------------------------------------------------------------------------------------------------------------------------------------------Sarcoidosis * A 27yo woman comes to your office with painful erythematous papules that occurred one day before your visit. The papules are red and tender. So FEV1 and FVC diminished but ratio of FEV1/FVC is the same. tuberculosis). but implies chronic). metastatic adenocarcinoma. Kveim test is a purified antigen from the granulomas of sarcoid patients. silver. gold. We don’t necessarily have information to know this is sarcoidosis. symmetric swelling of the knees.18 - . CNS involvement (treated with steroids). blow bottles. cancer. you would think emphysema. This causes a chronic inflammatory response. This is immotile ciliary syndrome. * Asbestos found in older building insulation. Kveim-Siltzbach) test is the equivalent of the PPD/mantoux test for TB. * Kveim (Nickerson-Kveim. bilateral hilar lymphadenopathy leading to lung scaring and eventually honeycombing pattern. skin lesions (lupus pernio on face.g. erythema nodosum on the lower extremities). If they are a smoker. Tissue should show non-caseating granulomas. DO NOT DISTRIBUTE . * Rarely will these patients respond to steroids. * Pneumoconiosis seen in the mining industry or heavy metal exposure. pneumococcal. * Patients may develop episodes of blood-tinged sputum or hemoptysis. * Smoking exacerbates and is superimposed on these diseases. cor pulmonale. and coal worker’s lung. Other causes of bilateral hilar adenopathy are granulomatous diseases (e. * Sarcoid causes scaring. bilateral lymphoma. influenza virus. hypercalciuria too. * Hypercalcemia seen in sarcoidosis due to elevated levels of vitamin D so absorb more calcium. * These patients are generally not smokers. then stop the steroids. so do a mediastinoscopy to biopsy nodes. chest physiotherapy. photophobia. remove patient from environment if still there. have patient quit smoking. Add in joint swelling and we could be talking about Crohn disease. infection is likely to be pseudomonas aeruginosa. * Sarcoid associated with Bell palsy. you see bilateral hilar lymphadenopathy. Think Kartagener syndrome (primary ciliary dyskineasia). clap on their back to get mucus moving. have them bend over. suctioning of the airways. Measure pre-steroid PFTs and post-steroid PFTs. finger clubbing (not specific. * Diagnosis is with tissue. Chest x-ray will show increased white markings (from scars). nickel. hemophilus influenza. The physical exam reveals low-grade fever. Pneumoconiosis. * Other disease involving the head that can cause blindness. silicosis. parotid gland enlargement. * Given a chest x-ray of a bronchiectasis patient where you see the liver impression on the right and gastric airbubble on the left. PFTs similar to restrictive disease. old building construction.

Restrictive disease. lungs are clear. 5000U subq q12h) as well as post-op anticoagulation. * Patient may be ambulatory but have dementia so they don’t leave bed. * Gold standard to determine if a patient has a DVT is a venogram.19 - . small round densities typically mid to lower lobes. Her respiratory rate is 26. you order a V/Q scan.52/25/75. you will see ventilation but no perfusion in a particular area. * Mesothelioma is a specific and rare cancer seen with asbestosis. * A Doppler is a valid initial approach in a pregnant patient. She has never been sick before. especially hip replacement). A PE usually originates from the deep veins of the legs or pelvis. DO NOT DISTRIBUTE . that is enough to start with anticoagulation. * If you see oral contraceptives (hypercoagulability due to estrogen) and sudden chest pain. thighs > calves. worse with deep breath. Silica fibers are released from rock blasting. rest of exam is normal. it is likely too late. only done if you have no choice.2*25 = 120. you may be forced to do more tests. * Patients with silicosis should get annual PPD testing. * To detect a V/Q mismatch. Say the Doppler is equivocal and the V/Q scan is equivocal. * A-a gradient: 150 1. But there is a clot blocking blood in the pulmonary artery. you should think about rheumatoid arthritis (Kaplan syndrome) and check rheumatoid factor.75 = 45 (normal < 15). The radiologist has a large list of criteria to determine probabilities. cancer. especially if a smoker. If you happen to get a biopsy. such as symmetric swollen joints possibly with hand involvement. * What is the first step in detecting a pulmonary embolus? Answer is V/Q scan (non invasive study). * The DVT risk for hip surgery is so high that standard of care includes pre-op prophylactic anticoagulation (subcutaneous heparin. * CXR shows calcification of the pleura (white areas). ventilation perfusion scan. So you need to do testing. clinical signs/symptoms of DVT. Primarily you see thick pleural bases. post-op. the alveolus is just fine. These patients are at increased risk for TB. no wheezing. the airway is just fine. * Silicosis is seen with rock mining. Normally there is a superimposed pattern of ventilation and perfusion. This is rarely necessary.g. * Another non-invasive test is a Doppler sonogram of the lower extremities. coughing. Drop PCO2 by 10. This patient is not taking any medications except oral contraceptives. digging quarries. digging tunnels. If you look down and see answer choices like venous Doppler. The test is painful. eggshell white. spiral CT scan. ventilation/perfusion (V/Q) mismatch. * What is the quickest test to determine if a patient needs treatment for a PE? Answer is Doppler. Other hypercoagulable criteria are not included in Wells. * Patients with coal miner’s lung who have joint complaints. previous PE/DVT. then you do the pulmonary angiogram. you know it is likely a question about pulmonary embolus. HR > 100. * 70-fold increase in primary lung cancer in asbestos exposure with concurrent tobacco smoking. is tachycardic. Then IV nuclear material is labeled to RBCs and another image is taken to determine perfusion. * A thrombus is a clot at its point of origin. * Treatment is to get patient to stop smoking. injection of dye into small vein of the foot with imaging to see the dye. CXR nodules favor the upper lobes (similar to TB). * By the time you think to biopsy a cancer. -------------------------------------------------------------------------------------------------------------------------------------------Pulmonary Embolism (PE) * A 32yo woman is brought to the ED with acute onset shortness of breath and pleuritic chest pain (sharp pain. * Pulmonary angiograms are used less widely now due to more acceptance of the spiral CT scan with contrast. there will be barbell shaped ferruginous body (asbestos fiber coated with iron-rich material). diagnosis found via occupational history. With intermediate. Results come as low. If there is a PE. thing PE. ABG shows mild evidence hypoxemia. * Patients at risk for DVT get anticoagulated (subcutaneous heparin) or get sequential compression devices (SCDs). Detected by biopsy only. * 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. pH goes up by 0. * Risk factors for pulmonary embolus (Wells criteria): immobilization (e. * Gold standard to detect a PE is a pulmonary angiogram. * Encourage patient to quit smoking. So there is an area that is ventilated but not perfused. * V/Q scan is not gold standard. ABG 7. * Patients develop interstitial lung disease. no rhonchi.Study Notes – Internal Medicine James Lamberg 28Jul2010 * No specific signs or symptoms.08. * Restrictive disease. Patient breathes in nuclear-labeled air and an image is taken to determine ventilation. such as use of oral contraceptives. * In a PE. An embolus is a broken off clot that traveled. intermediate. Answer is not mesothelioma. So the problem is with gas exchange. * Coal miner’s lung associated with mining coal. use subcutaneous heparin. or moving) that occurred while she was shopping. If there is a blood clot. PE is likely #1 diagnosis. waste of ventilation. or high probability of PE. and hemoptysis. So 120 . since the presence of DVT warrants anticoagulation. nearly always fatal. * Physical exam will reveal an absence of problems.

7. * Heparin works by potentiating antithrombin III effect. still in the presence of a clear lung exam. If for stroke or prosthetic valve. * Treat patient with IV heparin for about 5 days. Oral vitamin K will lower INR in 24-48 hours. Problem with PT test is control time varies too much. we need to reverse the effect of warfarin. Once the patient has a stable PTT. VII.20 - . So. Protein C has the shortest half-life. The fastest acting anticoagulation agent is IV heparin. it is teratogenic. May see signs of cor pulmonale acutely. right axis deviation on ECG. * If the pulmonary embolism makes it peripheral to the pleura. then we can give heparin. Prothrombin no longer measured directly. Protein C and S as well as antithrombin III (AT III) are necessary to prevent constant coagulation. Subcutaneous vitamin K not recommended. X. more specifically fresh frozen plasma (FFP). So we treat the patient with IV heparin for 5 days then send them home on subcutaneous heparin (10. we just follow the dose. recent CVA. * The problem with LMWH is that they are very expensive. increase heparin infusion rate. a qualitative problem. or ECG S1 Q3 T3 pattern (abnormal S wave in I. Heparin is not thrombolytic therapy. Examples are recent major surgery. * If patient bleeding with high INR. Start patient on oral anticoagulant (warfarin/coumadin) that they will stay on for the next 3-6 months. VII. If you’re at a PTT of 100. stop heparin for a few hours to let the level come down as patient is at high risk of bleeding. * Clots in strange places. give vitamin K. Aiming for time of 1. takes long flight across seas and is suddenly short of breath. You expect the patient’s own endogenous system (protein C. this is most likely a PE case. * FFP comes from other human beings thus it can come with infections and transfusion reactions. So. protein S. IX. even with a massive PE the CXR will be normal. You could see this on CXR possibly. like upper extremities (axillary vein) or in any artery. IV vitamin K will lower INR in 6-8 hours. * A patient has a positive V/Q scan with symptoms. this patient got pregnant and now is hypercoagulable due to estrogen. the pleura can infarct and cause a pleural rub.Study Notes – Internal Medicine James Lamberg 28Jul2010 * Patient is normally ambulatory busy businessman. IX. If INR is 5. If PTT low. * Warfarin works by inhibiting vitamin K dependent coagulation factors (II. So the first effect warfarin has is to make the patient protein C deficient. not specific or sensitive). Factor V Leiden causes activated protein C resistance. loud S2. as many drugs affect the same P450. “pro time”). so it will not break the clot. acute right ventricular heave.5 to 2. Treatment is anticoagulation. plus protein C). it is done by INR. antithrombin III) to break up the clot and after time the vessel will recanalize. * Patients with CHF are at increased risk for DVT/PE due to poor cardiac output and blood stasis. recent major trauma. X. * Check heparin level with PTT (partial thromboplastin time) test. so much so that we do not need to follow repeated PTT levels. Warfarin is contraindicated in pregnancy. you can get signs of right ventricular strain.5 times control. which will work within the hour. * If the patient has a high INR without bleeding. If control in assay is 30 seconds.5 times the control. and is not moving around much. increase oral warfarin dose to get them above 2 for the DVT. International normalized ratio (INR) range for a DVT is between 2 and 3. LMWH is a once a day dose. * Drug interactions are important with warfarin. If this patient does get a DVT. Warfarin inhibits protein C. Factor V is necessary for protein C to work. * So once PTT is 1. Keep patient on continuous heparin infusion. * Warfarin has a sizeable morbidity and mortality associated with it because there is variation in week-to-week or even day-to-day dosing. * If a large pulmonary vessel is clotted. So if INR is 1. we give factors II. has a baby pressing on her pelvic veins. * When do you need to know for sure that this is a pulmonary embolus. so they have more tendency toward hypercoagulability. and flipped T wave in III. Pregnancy increases risk for DVT. Even sitting in a car for a long trip. * We do not start warfarin at the same time as we start the heparin. DO NOT DISTRIBUTE . we have to regularly check INRs. distended neck veins.000U subq TID as we need 20k to 30k units daily). She has been gaining weight and stays at home most days. 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. think hypercoagulable state. * 25yo woman stopped taking her birth control pills because she is scared of clots after reading about them on the Internet. * Low molecular weight heparin (LMWH) has more consistent effect on PTT. So you want to prevent the clot from getting bigger. INR between 3-4. * Measure warfarin via PT (prothrombin time. * Factor V Leiden is the most common cause of thrombophilia. This is not the normal case. You do not think the patient is going to die from this clot. Q wave in III. so quantitative levels of protein C are normal. then we can start the warfarin. Heparin is given in bolus (say 5000U) then infusion (say 10 or 15U/kg) at say 1000U/hour. you want 45 to 75 seconds. recent duodenal bleeding ulcer.5-2. could be a few hundred dollars a day. P2 louder with inspiration. Heparin is safe during pregnancy. shorter than factor VII.

a post-op patient who got a DVT or a patient who got a DVT after a plane ride. so think of it as compressing the left ventricle. What if the patient gets another pulmonary embolism? Answer is place an IVC filter. so oxygen cannot diffuse through the fluid to the membrane. which the patient has already been started on. The lungs are flooded with fluid. * Giving these patients oxygen does not do much to fix hypoxemia. Catheter placed through RA. * Premature newborns get similar problems (gas exchange problem at the alveolar-capillary membrane) when born without enough surfactant. Physical exam reveals diffuse crackles. -------------------------------------------------------------------------------------------------------------------------------------------Acute Respiratory Distress Syndrome (ARDS) * 32yo man is admitted to the ICU with presumed gram-negative sepsis. but can’t anticoagulate. * Patient on ventilator. burns. For instance. others may be mesh patterned. or blood gas shows increasing hypoxemia. until he suddenly develops severe dyspnea. Hypotension in the setting of pulmonary embolus is an ominous finding. * Say the patient has a PE. real 60% oxygen into trachea with patient intubated. * What if the patient has a PE.Study Notes – Internal Medicine James Lamberg 28Jul2010 * Say patient has life-threatening PE. which helps to force the air through the fluid.g. * Risk of giving PEEP is blowing a hole in the alveolus. drowning. into outflow tract with balloon deflated. then we add PEEP (positive end expiratory pressure). you increase right-sided venous return at the expense of the left ventricle. like internal jugular or subclavian (IJ safer because further from lung). * ARDS also known as non-cardiogenic pulmonary edema. if there is enough time to save the patient. like a saddle embolus at the main pulmonary artery. you have to rule out cardiac so normal pulmonary wedge pressure and LV end diastolic. * Thus to prove ARDS. Inflating the balloon too much could rupture the pulmonary artery. On the catheter is a pressure transducer. barotrauma. * Oxygen toxicity can occur with FIO2 > 50%. Say patient got a DVT in the first month of pregnancy due to increased estrogen levels. which causes fibrosis. The patient seems to improve over the next day. * One sign this is a potentially fatal PE is that we are delivering 100% oxygen and the sats keep dropping. like CHF or an underlying coagulation disorder? Then we anticoagulate for as long as the risk exists. PEEP holds the alveoli open.21 - . * Treatment is intubation and delivery 100% inspired oxygen. Insert into a large vein. some are disk shaped with pores. So even if you intubate the patient and deliver 100% O2 directly into the trachea. left atrium has no input thus no LV output. compared with an unremarkable admission chest x-ray. Blood cultures grow pseudomonas sensitive to ceftazidime and ciprofloxacin. He is placed on double gram-negative antibiotic coverage and remains stable for the next 24 hours. * ARDS occurs in gram-negative sepsis. so we can measure the pressure in the pulmonary artery. resulting in hypotension. pulmonic valve. insert a pulmonary artery catheter (Swan-Ganz catheter). * As intrathoracic pressure gets increased with PEEP. Some IVC filters are shaped like an umbrella (IVC umbrella). and patient getting hypotensive. This causes a ventilation perfusion mismatch at the entire lung. RV. thus we do not stop the anticoagulation if we do not have to. Patient will become hypotensive. We have to protect the patient against future emboli. trauma with or without multiple PRBC transfusions. If an ABG shows PO2 low (like 45). CXR normal. the PEEP will continue to push air out. mediastinum shifts away. we diagnose and treat with the correct PTT then INR. Another sign is acute right ventricular failure with hypotension. recent major hemorrhage). So we put in an inferior vena cava (IVC) filter. causing pneumothorax. SVC filters can be placed as well. Answer for next step is to decrease PEEP. Give tissue plasminogen activator (tPA) or streptokinase (SK). * Why don’t we just give tPA in every patient? About 1% of patients getting thrombolytics die of a bleed. Or patient has major PE and a recent GI bleed. no blood will be there to transfer the oxygen into the system. Do you give tPA or streptokinase? Answer is emergently take patient to the OR or via interventional radiology (IR) to do an embolectomy. * To measure capillary wedge pressure (PCWP). An ABG shows hypoxemia and hypercarbia. This will lyse the clot. is hemodynamically stable. resulting in an intracranial bleed. Definition is PO2 < 60% on FIO2 > 60%. then we anticoagulate for the entire pregnancy. leading to a tension pneumothorax. * We anticoagulate the embolus 3-6 months if there is a reversible cause. In less common instances. What about patients who have an on-going risk. so it will acutely fail. narcotic overdose. About 10% of patients getting thrombolytics have a major bleed. but anticoagulation is contraindicated (e. The filter itself is thrombogenic. DO NOT DISTRIBUTE . * If you cause a pneumothorax and do not recognize it. the right ventricle is trying to pump against tremendous resistance. * Treatment for life-threatening PE is thrombolytic therapy. * Say patient had major PE then became hypotensive and fell. Diffuse alveolar densities are seen on CXR.

called facial plethora (Pemberton sign). you should worry that metastasis has traveled to the recurrent laryngeal nerve (outside lung). Patient will get swelling in face with redness. * Chronic smokers generally develop chronic hoarseness/laryngitis. patient hooked up to EEG. We get a continuous column of pressure at that capillary. Take chilled saline that you know the temperature and fluid amount. which is in continuous communication with the left ventricle. 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). * Catheter has a thermometer on the tip along with balloon and pressure transducer. Below 2. must get bronchoscope. and back to the pulmonary capillary. nearly all are unresectable. * Men: 2nd cause is prostate (1st if non smoker). * Post-obstructive pneumonia is when patient has recurrent pneumonia in the same location. * Cough with another symptom. not always successful. 5-year survival rate is about 5%. gets better. must do an open biopsy (can be done laparoscopically these days).2 L/min/BSA. drink more and more coffee and still falling asleep. So pulmonary edema with low LVED pressures suggests ARDS. Associated with paraneoplastic syndrome of hypercalcemia due to parathyroid hormone like substance secretion. It is not a popular test because the patient is trying to fall asleep while hooked up to all these devices. smokers usually cough. * If the lesion is somewhere in the middle. ECG. * Seen in obese patients. aortic valve is closed. * Major cause of sleep apnea is obstruction of the upper airway at the larynx and epiglottis. * A non-smoker that gets lung cancer is likely adenocarcinoma. blood-tinged cough. pulse ox. * More invasive treatment if CPAP fails is surgical intervention to open the airway. so no risk of barotrauma like in PEEP. That is because secretions cannot clear due to obstruction. respiratory rates measured. * Testing done in sleep lab. * The positive pressure in CPAP is being delivered to the mouth. * So we inflate the balloon. * You can also measure cardiac output via the Fick equation with a Swan-Ganz catheter. * Cardiac index should be > 2. 3rd is colorectal cancer. you can do a bronchoscopy and biopsy.2 is very poor flow. Maybe they have superimposed bronchitis. CXR 3 weeks later still shows a patchy spot. * Patient does not realize this is happening. If a patient suddenly develops hoarseness. * You can follow cardiac index to help determine how much diuretic or inotrope to give. it travels down and gets wedged in the pulmonary capillary. one can do a CT guided needle biopsy. This is a very non-specific symptom. post-obstructive pneumonia. 3rd is colorectal. * Treatment is with CPAP (continuous positive airway pressure) mask at night. the ventricle is maximally full. Testing is with laryngoscopy and patient phonating to determine if a vocal cord is paralyzed (ENT consult). * Most common initial presentation is a cough. So either the patient has daytime somnolence (fall asleep at my desk. look for a change in the cough. similar concept as PEEP. what if the pressure is 5mmHg? The low pressure suggests it is noncardiogenic pulmonary edema (ARDS). * Women: 2nd cause is breast cancer (1st if non smoker). So. but in cardiogenic pulmonary edema it is low. * Cardiac index may be normal or high in ARDS. so this is the left ventricular end diastolic pressure. * Say pulmonary capillary wedge pressure (PCWP) is 25mmHg with edema? That is cardiogenic. this implies unresectable cancer. Taking all lung cancers that present to the physician’s office. Patient gets pneumonia. * We have no good diagnostic test to improve survival in smokers who develop lung cancer.Study Notes – Internal Medicine James Lamberg 28Jul2010 * At the end of diastole. so more likely to be bronchoscopy with biopsy. If not cleared. Will have tremendous intolerable (to others) snoring. -------------------------------------------------------------------------------------------------------------------------------------------Lung Cancer * Most common cause of cancer death in both men and women is lung cancer. * Say LVEDP normally is 7-12mmHg. * If cancer is found and centrally located. * So any smoker with pneumonia you must follow CXR until it is clear. * If the lesion is peripherally. -------------------------------------------------------------------------------------------------------------------------------------------Sleep Apnea * Sleep apnea is cessation of breathing during nighttime sleep. occurring at least 10-15 times per hour and at least 10 seconds per episode. * About 5% of cases are central apnea where the issue is not in the upper airway but in the respiratory drive. like pleuritic chest pain. This is a difficult diagnosis at times. Thermometer tells you what the temperature of the blood is. * Once a patient has about 10% weight loss with a new lung cancer diagnosis. that pressure transmits back to the pulmonary veins. You inject the saline and the catheter measures continuous temperature. falling asleep while driving) or spouse notices loud snoring. * Superior vena cava syndrome implies a big mass in the chest is impinging the SVC.22 - . DO NOT DISTRIBUTE . the mitral valve is still open so the pressure is transmitted back to the left atrium. * Squamous cell carcinoma is generally centrally located.

so needle aspiration biopsy or thoracotomy to get tissue for diagnosis. look for lack of metastasis. papillary necrosis). best test is ultrasound of the kidneys.23 - . urethral stricture). * Pre-renal azotemia is due to poor perfusion of the kidney. they think you are bleeding to death (evolutionary response). Significance is back pressure damages kidneys. Eaton-Lambert syndrome. such as a large tumor causing obstruction. third-spacing into abdomen from pancreatitis). can progress to renal damage (acute tubular necrosis) and intrinsic renal failure. classic scenarios. -------------------------------------------------------------------------------------------------------------------------------------------Kaplan Videos (2001) – Nephrology with Dr. you can be sure we’re talking about Zenker diverticulum. * The greatest impact to reduce lung cancer rates is through education of teenagers before they start smoking. so high (concentrated) urine specific gravity and high (concentrated) urine osmolality. straightforward topics with obvious answers if you know the content. local extension into nearby organ. Barry Weiss. and anatomic like renal artery stenosis). poor cardiac output especially CHF). * The only good news about lung cancer is the rates are decreasing as people are smoking less and less. early SVC syndrome. * Tests for pre-renal azotemia include high BUN/Cr ratio (> 20) is the most important. esophagus). nephrotic syndrome). To determine if the patient can be cured. Causes include volume depletion (dehydration. so if a post-void scan shows 300mL of urine. * In low-flow states. Lab tests show creatinine of 3. and bladder (U/S KUB). DO NOT DISTRIBUTE . * 62yo man comes to the ED for nausea and vomiting. but 95% are not cured at 6 months and die. it was normal two months ago. bone involvement. so they retain lots of sodium to help build up intravascular volume. differentiated from myasthenia in that muscles improve with use (MG patients worsen with use). ureteral obstruction (tumors. and post-renal azotemia (outflow). intra-renal azotemia (intrinsic disease). MD -------------------------------------------------------------------------------------------------------------------------------------------Questions should be core. best considered as transient ischemia. * Tests for post-renal azotemia include prostate exam. A canoe trip in Connecticut. * Must be distinguished from intra-renal and post-renal azotemia because the treatments are very different. * Pre-renal azotemia is important because it represents low blood flow to the kidneys. but this is not a cure.g. * Post-renal azotemia causes include bladder outlet obstruction (prostate enlargement. so low urine Na+ (< 10-20) and low fractional excretion of Na+. The questions are not meant to trick the test taker. renal artery vasoconstriction (meds like NSAID. There are similar key words and patterns to know for nephrology. functional kidneys retain sodium to maintain vascular volume. functional kidneys will concentrate urine to retain fluid in the body. you should worry about outlet obstruction. * Intra-renal failure is damage to the kidney itself. ACE-I. < 10 is intra-renal. In low flow states. * 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. liver. So by the time you make the diagnosis. associated with SIADH (hyponatremia with euvolemia). stones. Post-renal could also have a BUN/Cr of 10-20. * You expect about 50mL of urine left in bladder after urination. Signs of metastasis would be malignant pleural effusion. cardiovascular (hypotension. catheterization or bladder scan (to detect post-void residual urine volume).Study Notes – Internal Medicine James Lamberg 28Jul2010 * Small cell (oat cell) carcinoma generally centrally located. it’s too late to cure. ureters. -------------------------------------------------------------------------------------------------------------------------------------------Acute Renal Failure * If you’re told a patient has bad breath. or FENa. These are classic cases. 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. pelvic tumors. (< 1%). decreased oncotic pressure (low albumin edematous states like cirrhosis. * Small cell cancer metastasizes early. * You can have local nodes and be cured with resection only if the nodes are on the same side of the cancer.6. * Eaton-Lambert syndrome is neuromuscular end-plate injury. * Some of the blood flow into the kidney is prostaglandin-dependent and NSAIDs block prostaglandin. * Patients may still be resected for palliative measures. you must assume there has been micro metastasis and thus resection is not an option for cure. we’re talking about Lyme disease. burns. * Normal BUN/Creatinine ration is 10 to 20. If untreated. also called intrinsic renal disease or acute tubular necrosis (ATN). brain involvement. * What happens is the kidneys don’t get enough blood. thus urine sodium is very low. * Non-small cell lung cancer can be palliated with chemo and radiation. local contiguous structures (e. * Even if you have a tiny lung cancer and a single node on the contralateral mediastinum. inflow issues like circulation).

* Elderly man dropped pen under bed and went to go retrieve it.Study Notes – Internal Medicine James Lamberg 28Jul2010 * 62yo man comes to the ED with nausea and vomiting. in intra-renal BUN/Cr is low with high urine sodium. creatinine was normal now is 2. you treat the cause (most causes you give them fluid. * Allergic interstitial nephritis is an allergy reaction to a drug. methotrexate. cryoglobulin disease. -------------------------------------------------------------------------------------------------------------------------------------------Intra-Renal Disease: Tubulo-Interstitial Disorders * Acute tubular necrosis (ATN) occurs in prolonged ischemia (hypotension. rifampin. mitomycin C). sulfonamides. Key findings are urine eosinophils. it just leaks out. abnormal urinary sediments (hematuria. * In summary. polyarteritis nodosa. lithium). like furosemide. vitamin C). myoglobin (rhabdomyolysis). Follow azotemia algorithm. The broken down muscle tissue releases myoglobin. Renal biopsy is the most definitive test. * Phases of ATN are prodromal.6. granular and RBC. -------------------------------------------------------------------------------------------------------------------------------------------Glomerulonephritis * Intra-renal disease has high urine sodium (> 20) and high FENa (> 1%). you’re faced with a high creatinine level that is new (azotemia). penicillins).g. urine osmolarity < 350. These patients will lose their oncotic pressure and develop edema. if you don’t see pre-renal or post-renal problems. young children). thrombotic thrombocytopenic purpura. diabetes. toxins (radiologic contract. which goes through the renal tubules and is toxic to the tubules. treat it. peripheral eosinophilia. arterial insufficiency/occlusion.24 - . protein (multiple myeloma with Bence Jones protein). cyclosporin. follows strep skin or throat infection). urine Na > 20. antibiotics (aminoglycosides. BUN/Cr is high. * If patient on diuretics. Berger disease (IgA mesangial deposition after viral illness. Presentation is fever. this is 4+ dipstick positive with grams on measurement. Had a sore throat a week before. So. -------------------------------------------------------------------------------------------------------------------------------------------Intra-Renal Disease: Glomerular Disorders * Vasculitis causes include Wegener granulomatosis (lesions in lung. so urine specific gravity < 1. then that may cause high urine sodium do don’t assume intra-renal failure. Think Wegner and order ANCA. FENa > 1%. low specific gravity. high specific gravity. SLE). Also has kidney issues. Answer to why they are failing is pre-renal azotemia. it is most likely intrinsic renal. Osm < 200. Typical drugs are beta-lactams (e. cephalosporins. FENa < 1%. and ANCA anti-neutrophil cytoplasmic antibodies). * Nephrotic syndrome occurs in vasculitis and glomerulonephritis. Osm > 500. oxalate crystals (ethylene glycol. nasal. most commonly a cephalosporin. not done often in clinical practice because of risk. Casts come from the kidney. * Treatment for pre-renal azotemia is fluids.g. radiation nephritis. urine Na < 10.028. If you find post-renal. hypercalcemia (hyperparathyroidism). hypertension. RBC casts). * So in pre-renal BUN/Cr is high with low urine sodium. * Patient has lung lesions and recurrent sinus infections. uric acid crystals (chemotherapy. * Teenager presents with intrinsic renal disease. cancer drugs (cisplatin. allopurinol. Can’t concentrate urine. * Drugs and toxin causes include analgesics (NSAIDs). Urine sodium >20-40 because kidneys are failing so they lose the ability to protect sodium.015. rash. collagen vascular disease (e. Treatment is stop drug and short-term steroids to cool down reaction. heavy metal poisoning (lead. Alport syndrome (renal failure and deftness). think allergic interstitial nephritis and look for what drug needs to be stopped. pigments like myoglobin). Massive proteinuria > 3. Also look for casts. Once uncer the bed he couldn’t get out. * Algorithm: First thing to do is exclude pre-renal azotemia by looking for lack of BUN/Cr > 20. urine Na+ 6. mercury. If you see urine eosinophils. BUN 82. * Glomerulonephritis causes include post-streptococcal (do ASO titer. and post-oliguric (diuretic). oliguric (when kidney starts showing changes). cephalosporins. previously called “shock kidney”). * Intra-renal azotemia: BUN/Cr is < 10-15.5g/day. expired tetracyclines leading to Fanconi syndrome). amphotericin B. Answer is order ASO titer. Next thing to do is exclude post-renal azotemia by sonogram and/or catheter looking for lack of obstruction. DO NOT DISTRIBUTE . gold. prolonged pre-renal azotemia. Neighbor realizes man hasn’t come out of the house for a few days and finds the man stuck under the bed. Patient has been lying on the big muscles of the legs for a long time with no good circulation. drugs like aminoglycosides and amphotericin B. * Patients who have diabetes (and are taking metformin) and get contrast dye should have the metformin stopped prior to the procedure. Henoch-Schonlein purpura. or treat CHF or renal artery stenosis). tumor-lysis. Has orthostatic hypotension. Goodpasteur syndrome (anti-GBM antibodies in lung and kidney). urine specific gravity 1. urine sodium is low so kidneys are retaining it. * Deposition disease causes include hemoglobin (hemolysis). If you find pre-renal. sinus. Signs of intra-renal disease are BUN/Cr < 10. * Infection causes include pyelonephritis with WBC casts and bacteria in urine. gout).

25 - . BP 11/70. glomerulonephritis (15%). BP 140/90 (pretty high). not bicarbonate for acidosis. polycystic kidney disease (5-10%).2. So we ruled out pre-renal with urine originally. * Best test to determine the type of glomerulonephritis causing the nephrotic syndrome is renal biopsy. He has a recent sore throat. * Some key words in renal disease to remember. You rule-out pre-renal and post-renal.023. This is an indication for dialysis. afebrile. creatinine 3. * Urinalysis can show infection (WBC. * Most common causes are diabetes (30-50%). Exam is normal except large prostate. uric acid (gout). hypertension (10-25%). think nephrotic syndrome. This causes secondary hypoparathyroidism. Most common cause of dialysis is diabetic kidney disease. Could have hypoperfusion due to NSAIDs. Cardiac exam shows peripheral edema and signs of CHF. Could have BPH or cancer causing large prostate obstruction. think glomerulonephritis. Urine sg 1. 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. * So you have a patient with azotemia. so likely dehydrated. RBC casts. needs dialysis. All acute manifestations are indications for dialysis. BP 110/70. Hypermagnesemia occurs due to failure to excrete magnesium. but still need to rule out post-renal. and can lead to them being obtunded and even comatose. we assume renal disease and follow that. but a 62yo man probably has a large prostate due to BPH. Heavy proteinuria. * 14yo boy comes to see you with swollen hands and legs. and unknown (10-15%). You see blood in the urine and RBC casts. It is determined by the presence of acute manifestations. Metabolic acidosis occurs but kidneys cannot compensate. Hypocalcemia with osteopenia occurs. no casts. * 62yo man comes to the ED for nausea and vomiting. not furosemide for CHF. Patient has high pulse and nausea with vomiting. exam confirms edema. * Chronic manifestations of ESRD occur whether or not you are on dialysis. not to mess around with other treatment. Urine shows proteinuria and RBC casts. myeloma (Bence Jones). Urine Na+ 9. What is the next step though? Answer is sonogram to exclude post-renal azotemia. * Need for dialysis is not determined by creatinine level. Fluid overload occurs to the point of pulmonary edema and the kidneys cannot remove the fluid. myoglobinuria (blood on dipstick due to myoglobin. If you look at the BUN/Cr. pulse 110. Hyperlipidemia also seen. RBCs. drug hypersensitivity (eosinophils). Best initial treatment is fluids. Creatinine is 5. Once that is out of the picture. no medications. the combination of accelerated hypertension and hyperlipidemia leads to accelerated atherosclerosis leading to cardiovascular disease. This is post-streptococcal glomerulonephritis. so need dialysis. needs dialysis. Best test to establish a diagnosis of nephrotic syndrome is 24-hour urine protein. high creatine kinase CK in blood). So pre-renal azotemia. not kayexalate for potassium. start to occur when the creatinine gets to about 3. bacteria). In order to survive. Creatinine is 3. BUN/Cr is close to 10. vomiting.Study Notes – Internal Medicine James Lamberg 28Jul2010 They can run their total albumin way down and get anasarca (“marshmallow man” appearance). What blood test would be most helpful for confirming diagnosis? Answer is ASO titer.25-dihydroxy vitamin D. This is likely intrinsic kidney (intra-renal) azotemia. it’s 20 plus concentrated urine. * Dialysis can be done via blood (hemodialysis via a machine) or peritoneal dialysis (fluid instilled into peritoneum then removed). What is the best treatment for this patient? Answer is dialysis now. think drug reaction like cephalosporins. * Acute manifestations of ESRD include hyperkalemia (look for peaked T-waves on ECG). you need dialysis or a transplant. Exam normal except large prostate. Accelerated hypertension (renin-angiotensin action) occurs and is a big deal because it may be hard to control blood pressures. * 62yo man comes to the ED with nausea and vomiting.6 (new). Pericarditis occurs due to toxins causing inflammation of the pericardium and build-up in the pericardial sac of fluid. Dipstick is positive for protein and patient has edema. Encephalopathy occurs at to high creatinine levels. BUN 72. glomerulonephritis (RBC casts). no RBCs. urine sg 1. Could have bladder cancer or kidney stones due to RBCs in urine.6 (new) and is on NSAIDs. -------------------------------------------------------------------------------------------------------------------------------------------End Stage Renal Disease (ESRD) * ESRD is renal failure that is incompatible with survival. High triglycerides think nephrotic DO NOT DISTRIBUTE . usually asymptomatic. This is a clue up front because most people on dialysis get it every 2-3 days. Patient has nausea. and shortness of breath. BUN 41. nephrotic syndrome (lots of protein). ECG shows tall peaked T waves. * Best initial test to distinguish causes of intrinsic renal disease is a urinalysis. bicarb is 16 (metabolic acidosis). Immunosuppression occurs so increased infections. can’t dilute urine even though he is vomiting/dehydrated. How do you prove it is nephrotic? 24h urine protein. Pruritus occurs presumably due to toxins circulating in the blood that are normally excreted by the kidney. calcium is leached from bone causing osteopenia. There is a lack of 1. * 62yo dialysis patient returns from a 4-day fishing trip and feels poorly. which is involved in calcium reabsorption in the GI tract.004. Eosinophils in urine. Anemia occurs due to lack of erythropoietin production in the kidneys. Urine Na+ 42. pulse 110. so must get dialysis. What is the best initial treatment? You may be tempted to pick sonogram due to outlet obstruction.

there is less space for the sodium and water component of blood. diarrhea. volume depletion. Diagnoses to consider are congestive heart failure. May be a drug side effect. When protein/lipid increase. There is a magnitude effect. Serum osm is 292 (normal). sweat. drug side effect. hypoaldosteronism. diuretics. adrenal. glucocorticoid deficiency. Thus adjusted sodium is 136. so sodium is actually 129 adjusted. there is less sodium even though the concentration has not changed. so the patient’s volume status. Labs show glucose of 402. the patient is fluid overloaded and the cause is almost always an edematous condition. Normal blood osmolality is between 280 and 300. think pre-renal give fluids. * Patient presents with weakness. or a simpler but less perfect method is 2*Na + 10). * Hyponatremia mild or gradual change the patient will most likely be asymptomatic.26 - . * Low osmolality with hypervolemia. * Pseudo-hyponatremia can occur also with normal osmolality. So again. Sodium is gained. with a normal amount of sodium. in the healthy patient there is a small amount of protein/lipid per block of blood. SIADH. salt-wasting nephropathy (renal failure). brain disease. Extrarenal loss (urine Na+ < 10) due to GI loss from vomiting. and burns. * With normal osmolality pseudo-hyponatremia.8 difference for sodium. sodium is 128. Hemoptysis. the patient’s sodium is not truly low thus do not treat the sodium. normal volume states. * Causes of SIADH include lung disease. kidney. water intoxication (> 12-20L/day. including cirrhosis and congestive heart failure. low volume status assessed with tachycardia and orthostatic hypotension. thyroid function. High volume status assessed with edema. and hypothyroidism.2 (normal).Study Notes – Internal Medicine James Lamberg 28Jul2010 syndrome. sodium of 131. Say glucose is 342 and sodium is 126. If ECF is low (hypovolemia). so 3*1. showing hyponatremia (diluted) and hyperglycemia (from the dextrose). If the ECF is normal (euvolemia). 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. there are multiple causes including SIADH. symptoms include headache and confusion. In this case. Radiologic contrast. the next step is to measure the extracellular fluid volume. think Goodpasteur. * If the ECF is high (hypervolemia). Does the glucose explain the level of hyponatremia? Here.6 per 100mg/dL increase in glucose. ADH is secreated causing the patient to retain fluid and excrete concentrated urine. Emergency treatment is hypertonic saline (3% or 5%). that glucose accounts for about 3. hyper-proteinemia was ruled out. the patient has fluid loss with causes including GI. hyponatremia with normal osmolality (high lipids or protein). or due to skin loss from burns. So hyper-triglyceridemia is next. the glucose is about 300mg/dL high. So in hyperglycemia. * Low osmolality with hypovolemia. Blood osm is low/dilute. treat the glucose. and hyponatremia with low osmolality (true hypoglycemia. sweat. DO NOT DISTRIBUTE . * First step in determining why a patient is hyponatremic is determining the osmolality. With severe or rapid change. bowel obstruction.8. * SIADH has urine osmolality inappropriately high in the face of hyponatremia with low serum osmolality. * Hyponatremia with high osmolality caused by increase solute in the blood. symptoms include seizures. So per unit of blood. think acute tubular necrosis (ATN). Causes osmotic fluid shift from intracellular space into the blood. * Causes of hyponatremia include pseudo-hyponatremia. coma. BUN/Cr > 20x normal. accompanied and exceeded by secondary water gain. -------------------------------------------------------------------------------------------------------------------------------------------Electrolyte Disorders: Hyponatremia * Hyponatremia is arguably the most common of the sodium and potassium abnormalities seen in the hospital. glucose is 142. Osmolality can be determined by direct measurement (best) or by calculation (osmolality = 2*Na + glucose/18 + BUN/2. * Hyponatremia algorithm: once we rule out high osmolality and normal osmolality. edematous conditions.6mg% sodium per 100mg% glucose). * Patient presents with diabetes. Urine Na+ < 10. multiple causes). With moderate change. where sodium level measures low but artifacts from other substances make it appear low. We have low sodium with normal osmolality. * Low osmolality with euvolemia. also known as psychogenic polydipsia). What test will show the cause of the patient’s hyponatremia? Answer is serum lipids (triglycerides). Total protein is 7. where sodium falls 1. such as in high osmolality of hyperglycemia (1. tube drainage. Thus sodium is normal so the glucose explains this pseudo-hyponatremia. * “Real” hyponatremia is lab hyponatremia (from a basic metabolic panel) with low osmolality. multiple myeloma). lab artifact from hyper-trigleridemia or hyperproteinemia (e. neoplasm-related (most common is small/oat cell in the lung). nephrotic syndrome. and hepatic failure or cirrhosis. So the glucose does not explain all of the drop in the sodium. urine osm is high/concentrated.2 in sodium drop. Normal renal. * Hyponatremia with high osmolality (hyperglycemia). lab shows osmolality is low. usually glucose.g. Renal loss (urine Na+ > 10) due to diuretics. think pre-renal and give fluids.6 is 4. Fluid shifted into blood dilutes Na+ level.

phenothiazines.g.g. and chlorpropamide. * Rare causes of hypokalemia include hyperaldosteronism. meaning urine output drops and becomes more concentrated. If you correct the sodium too rapidly. also medication such as diuretics causing renal loss. used in labor induction. * Treatment of nephrogenic diabetes insipidus is to give thiazides or NSAIDs. NSAIDS increase prostaglandin (PG1). * What is the most common cause of hypernatremia? Answer is dehydration. which impairs urinary concentration ability. high and normal osmolality are artifacts of high glucose/lipids/protein. give vasopressin in the form of desmopressin (DDAVP) usually intranasal or sometimes subcutaneous or IV. How do you determine the cause? You need osmolality level and volume status. NSAIDs. * Treatment of central diabetes insipidus is to correct the underlying problem if possible (e. glucose 342. or Cushing syndrome from adrenal excess. resulting in quadriplegia. the problem is the kidneys (nephrogenic DI). like Conn syndrome primary hyperaldosteronism from renal disorder. If there is no response to the ADH. cyclophosphamide. then the problem is in the brain (central DI). Causes include diarrhea with loss of potassium in the stool. The urine will not change concentration either. the furosemide with loss of potassium in the urine. DO NOT DISTRIBUTE . confusion. moderate include muscle weakness. the patient is given ADH. digitalis/digoxin toxicity is potentiated. MAO inhibitors. Fluoxetine and chlorpropamide can cause SIADH. stop drug). think about diabetes insipidus. Received multiple albuterol treatments in the ED (emergency department). muscle cramps. Then. * Drugs that increase ADH action include chlorpropamide. clofibrate. low serum osm. In diabetes insipidus. lithium. Thiazides cause Na+ depletion and water resorption in the kidney. brain tumor). If there is a response to the ADH. * Treatment for dehydration is isotonic fluids with slow correction of sodium (1mEq/2h). chlorpropamide. * Drugs that mimic ADH function include oxytocin. restrict fluids. Now has increased SOB (shortness of breath). furosemide with normal saline (to raise blood sodium). and less commonly in diabetes insipidus (DI) where water loss is up to 20L per day. phenothiazines. fluoxetine. tolbutamide. * If you think the patient has DI. do a water restriction test.Study Notes – Internal Medicine James Lamberg 28Jul2010 *Drugs that increase ADH secretion include TCAs.g. * Treatment is to reverse the cause if possible (e. What are the possible causes of hyponatremia? Vomiting could cause dehydration. Hypothyroid can cause ADH syndrome. children). * 82yo man presents with 1 week of vomiting and 2 days of confusion. the urine volume will decrease with time and the urine output will be more and more concentrated. or Bartter syndrome from volume depletion secondary to impaired renal resorption of NaCl. albuterol) that increase potassium entry into cells. * Key points about hyponatremia: determine serum osmolality. * 73yo man with COPD and CHF has had diarrhea for 3 days. * Correcting hyponatremia too quickly can cause central pontine myelinolysis. -------------------------------------------------------------------------------------------------------------------------------------------Electrolyte Disorders: Hypokalemia * Hypokalemia common causes are GI loss from diarrhea. The more appropriate term now used is osmotic myelinolysis. * Symptoms of hypokalemia if mild are asymptomatic. carbamazepine. * Drugs to pay attention to here include TCAs. and coma. vincristine. carbamazepine. Takes thyroxin. cyclophosphamide. beta-agonists (e. and if severe and can’t find a reversible cause then demeclocycline or lithium. vinblastine. * If you cannot correct the sodium. and non-specific T and U wave changes. high urine osm. At any level of hypokalemia. there is no change in urine volume because there is no ADH to do it. -------------------------------------------------------------------------------------------------------------------------------------------Electrolyte Disorders: Hypernatremia * Hypernatremia is likely the least common of the sodium and potassium abnormalities. You also need urine sodium if volume status is low. Identify three possible causes of hypokalemia. In a normal person. vincristine. * Symptoms include lethargy. Other causes include licorice in high quantities due to mineralocorticoid effect of glycyrrhetinic acid. Meds include furosemide and albuterol. it can cause seizures due to cerebral edema. and commonly occurs in GI loss from diarrhea (e. and insulin that increases potassium entry into cells. theophylline. DI can occur due to central causes (idiopathic. * Diagnosis of SIADH is accomplished by seeing hyponatremia. seizures. With severe hypokalemia. * Emergency treatment for serious hyponatremia is hypertonic saline. fix pneumonia. and has pneumonia. * Causes include fluid loss in excess of Na+ loss commonly occurs in insensible loss from sweat (extreme exercise). fluoxetine. narcotics. tube drainage. with low osmolality you need to determine ECF. Sodium is 126.27 - . tumor) and nephrogenic causes (lithium. various renal diseases). High glucose could cause pseudo-hyponatremia.g. Get a urine osmolality if volume status is normal. and the albuterol with increased cellular resorption of potassium. cardiac arrhythmias occur. burns.

anxiety (acute pain. An excessive rate causes cardiac conduction defects including heart block and/or asystole. They still have potassium in their body but it is no longer in the circulation where it would induce cardiac arrhythmia. rhabdomyolysis. Exam shows orthostatic hypotension. never overcompensation. sudden cardiac conduction defects preceded by classic ECG changes (talk pointed peaked T-waves). also with bicarbonate as the alkalosis drives potassium into cells. This is respiratory alkalosis. ABG shows 7. IV replacement maximum is 10mEq/hour via peripheral IV or 20mEq/hour via central line. Labs reveal creatinine increased to 4. low chloride. Last step is to get rid of the potassium from the body. HCO3 rises with time to compensate almost back to a normal pH. leading to falsely high potassium levels. Pickwickian (obesity hypoventilation syndrome). K+ out). * Respiratory alkalosis will have increased pH. with compensatory slowing of respiratory rate and increase in PCO2.37 is acidosis and pH > 7. HCO3 unchanged because not enough time. Common causes of H+ loss include prolonged vomiting or other GI loss and diuretics (H+ and Cl. She presents for a routine checkup. * Metabolic alkalosis is a chronic process. potassium sparing diuretics. decreased PCO2. or asthma. and HCO3 of 33 is high. * Metabolic alkalosis is either a loss of H+ or a gain of HCO3.interchange). You get HCO3 (normal 20-28). and if sustained the kidneys will retain HCO3 in an attempt to lessen the acidosis. Patients needs treatment if ECG changes present. This can also occur if blood is drawn proximal to a running IV drip that contains potassium.28 - .52/25/PO2/27/99%. ACE-inhibitors). DO NOT DISTRIBUTE . Drives down the PCO2 with no time for metabolic compensation. This is metabolic alkalosis defined by high pH and high HCO3.43 is alkalosis. Electrolytes show low potassium. ABG also gives O2 and PO2. Movement of potassium from cells into the blood can cause hyperkalemia. PCO2 at 25 is low. could be renal failure. these changes are rapid. complains of fatigue. acute pulmonary disorder (pulmonary embolism. * Respiratory acidosis has decreased pH. should be above 90% normally. O2 sat typically in mid-90s. increased PCO2. How will you treat this? * Treatment should start with protection of the heart. occurs in acidosis (H+ into cells. So PCO2 of 47 is high. * 24yo female comes to the ED feeling like she is suffocating. pain attack). Acute causes include narcotics. Another causes is deceased renal excretion from renal failure or medications like spironolactone and ACE-Is. This is uncommon except in conjunction with certain medications (e. * Arterial blood gas (ABG) gives you pH. Potassium is one of the chemicals used for lethal injection because it causes heart block and asystole. * Symptoms include weakness that increases with potassium level.42/47/PO2/33/97%. has tightness in her throat and chest. Chronic causes include COPD. an inability to blow off CO2. such as an error in the hospital with excessive potassium administration. Why did her potassium become high? There are a number of reasons include the ACE-I. Could be a patient on birth control pills with acute pulmonary embolism. pneumonia). * 67yo woman with HTN is on HCTZ. where you can determine if this is acidosis or alkalosis. * 67yo woman with diabetes and hypertension is on glyburide and ACE inhibitor. This is a lung problem. A pH < 7.g. Common causes of HCO3 gain include NaBicarb ingestion (multiple antacid pills) and milk-alkali syndrome (CaCO3). Either way it is a lung problem.6.4 +/. which can vary by the altitude you live at. RR is 36.03. with bicarbonate working as a metabolic buffer. likely due to the hyperventilation.5 and potassium is 6. Hemolysis of cells causes the potassium to be released from the cells. This is done with glucose and insulin. -------------------------------------------------------------------------------------------------------------------------------------------Acid-Base Disorders * A normal blood pH is 7.Study Notes – Internal Medicine James Lamberg 28Jul2010 * Treatment of hypokalemia is done by replacing potassium. acute COPD. * Respiratory alkalosis is caused by hyperventilation. * Metabolic alkalosis has increased pH. She appears anxious. Hypoaldosteronism and adrenal insufficiency are other cause. Hyperventilation lowers PCO2 and breath holding or shallow respirations will increase PCO2. This is done with cation-exchange resin (kayexalate) or dialysis if renal failure. respiratory rate slows to raise PCO2 thereby increasing pH almost back to a normal value. Whenever possible. * Respiratory acidosis caused by hypoventilation (acute or chronic). early aspirin toxicity. replace orally. HCO3 unchanged because not enough time. Give CaCl or Ca++ gluconate infusion. low sodium. The PCO2 being high is respiratory compensation. ABG is 7. obesity.0. * What if the patient above had an O2 sat of 76%? This is not acute anxiety or panic attack. increased HCO3. -------------------------------------------------------------------------------------------------------------------------------------------Electrolyte Disorders: Hyperkalemia * Causes include increased potassium intake. You get PCO2 (normal 35-45) and should determine respiratory rate/volume. and sleep apnea. these changes are slower (2-5 days). Next step is to lower the potassium level by driving potassium into the cells. and rarely familial periodic paralysis. Pseudo-hyperkalemia can occur as an artifact from venipuncture or cell lysis from shaking the blood tubes.

ABG shows 7. How do we know this is not primary metabolic alkalosis (i. Treatment is mineralocorticoid replacement. Pupils small. idiopathic hypercalciuria.37/5/PO2/34/90%. ethylene glycol. iron/INH. Wilson disease. vitamin D intoxication). Inability to acidify urine. either high-anion gap (anion gap) or normal anion gap (nonanion gap). urine would be inappropriately high pH in RTA. Treatment is oral bicarbonate. so normal anion gap (11 +/. Treatment is volume restriction. has altered mental status. Chloride levels are unaffected “normochloremic. * Anion gap < 14 (normal) usually caused by HCO3 loss in GI tract or urine or inability to excrete acid in urine. urinary pH typically > 5. Is this acidosis or alkalosis? Answer is acidosis. destructive bone disease (myeloma. diabetic ketoacidosis. fludrocortisone. and loss of base (HCO3). As compensation. Her PCO2 is high. uremia.37 is not alkalosis.g. and struvite have calcium and are radio-opaque. Is this metabolic or respiratory? Answer is metabolic acidosis. * Metabolic acidosis is the most complicated of the group. * Must determine which type of metabolic acidosis. Diagnosed by high urine sodium with salt restriction (salt restriction test). amphotericin B. vitamin C excess. Inability to absorb bicarbonate until levels very low. Renal failure causes inability to excrete organic (non-HCl) acids. * Type 1 RTA occurs in distal tubules of the kidney. phosphate. decreased HCO3.3). Common causes are diarrhea and renal tubular acidosis (RTA). * High anion gap acidosis is an excess of non-HCl acid. klebsiella. and increased respiratory rate as compensation in an effort to blow off PCO2 thereby increased pH almost back to normal. Lactic acidosis is due to overproduction of lactic acid. * Metabolic acidosis is a relative increase in the quantity of acid.” There are four major causes: ketoacidosis (alcoholic. paraldehyde/phenformin. This is a narcotic overdose with respiratory acidosis due to hypoventilation. * Renal tubular acidosis key clue is the inability to acidify urine. * 72yo woman has COPD worsening over weeks. with causes including addition of acid. * Metabolic acidosis has decreased pH.g. What would be the best test to distinguish diarrhea from RTA? Answer is urine pH. * Main causes of uric acid stones include gout. others). Diagnosed by seeing bicarbonate lost in urine in the face of acidic blood. * Main causes of calcium oxalate/phosphate stones include increased calcium absorption (sarcoid. This is metabolic acidosis as bicarb is low. Intoxication causes addition of non-HCl acids. metastatic cancer). ABG shows 7. * MUDPILES: methanol. hyperparathyroidism. Anion gap = (Na + K) – (Cl + HCO3). ABG shows 7. are radiolucent and may not be seen by CT or other x-ray. hematologic malignancies). * Oxalate stones account for about 70%. * Anion gap > 14 caused by overproduction or under-excretion of an acid other than HCl. hyperoxaluria (fat malabsorption as fat binds to calcium. Anion gap is normally 11 +/. diabetic. * 72yo man has 4 days of diarrhea and presents to ED with weakness. Presents with hyperkalemia. PCO2 being low is compensatory. pseudomonas). methanol wood alcohol. Comes to the ED because she is becoming gradually SOB. Normal anion gap acidosis is excess HCl or loss of HCO3. vitamin D deficiency. which should be acidic (< 5. urate about 5%. the body does not overcompensate. cysteine rare.29 - . Nevada). Fanconi syndrome.e. What is the most likely cause of the this patient’s normal anion gap metabolic acidosis? Most likely diarrhea. leaving oxalate for excessive absorption). struvite about 5-10%. * Five kinds of stones: calcium oxalate (most common).31/30/PO2/17.4) in the presence of blood acidemia. DO NOT DISTRIBUTE . Seen in myeloma. Urate may not be seen on plain x-ray. HCO3 18. lactic acidosis. What is the anion gap? Gap is 12. occurs rapidly. Arizona. more common in desert southwest (e. starvation). * Ketoacidosis is due to overproduction of ketone bodies.9. inability to excrete acid. so 8-14. lithium. alkaline urine favors crystallization of struvite and can result in large stones (staghorn calculi). * Type 4 RTA occurs due to hypoaldosteronism. K 2. so likely a CO2 retainer with the COPD. renal failure (uremia). ABG shows 7. inc HCO3 with inc PCO2 compensating)? We know this because the pH of 7. * Oxalate. lactic acidosis.4 or even overtly alkaline.29/29/PO2/17/97%. Diagnosed by giving acid load/challenge test and still can’t acidify urine. cysteine (rare). Seen in kidney stones. Needle tracks on arms. sickle cell. Occurs with aldosterone or adrenal insufficiency and diabetes.Study Notes – Internal Medicine James Lamberg 28Jul2010 * 27yo man found unconscious on the street. phosphate about 10%. uric acid. tissue breakdown (e. Respiratory rate is 7. salicylate. body is breathing fast to bring down PCO2. Could be RTA. * Main causes of struvite stones include infection with urea-splitting bacteria (proteus most common.3. calcium phosphate. magnesium/ammonium/phosphate (“triple phosphate” or struvite).28/56/PO2/28/84%. Cl 113. * Type 2 RTA occurs in the proximal tubules of the kidney. * 17yo with diabetes has not been taking his insulin. salicyclates. or intoxication (ethylene glycol. Lytes are Na 140. -------------------------------------------------------------------------------------------------------------------------------------------Kidney Stones (Nephrolithiasis) * Urolithiasis occurs in 1-5% of the US population.

Tells you that father and cousins had a similar problem and both died of hypertension-related renal failure. hyperparathyroidism (serum Ca level. no longer test of choice. do spiral CT. bladder x-ray) is useful for patients with known stone disease. * 26yo female presents with sudden onset of severe flank pain radiating to groin. Creatinine is 1. Pain medication may be one of the first priorities. symptoms develop in 20s and 30s including pain from kidney size pushing on renal capsule. destructive bone disease (treat problem). spleen cysts. or what is the best test to confirm diagnosis? Answer is non-contract helical (spiral) CT scan. hematuria. bowel prep needed for good pictures. high blood pressure via RAAS. * For small stones (<5mm) in lower ureter is observation. Can be single or multiple. half have ESRD by age 60. Answer is urinalysis for hematuria. then do sonogram. To do this you strain the urine and send for urinalysis. with nausea and vomiting. fat malabsorption (history. vitamin C excess (history).Study Notes – Internal Medicine James Lamberg 28Jul2010 * Kidney stones present with severe flank pain radiating to the groin. * PKD manifests with hypertension in the kidneys. 10% are sporadic mutations without family history. diagnose symptomatic patients. What is the next step in determining diagnosis. What is the best test to make a diagnosis? Answer is renal ultrasound to rule out PKD. pain onset often sudden.5cm) stones. * Percutaneous nephrostomy is used for obstructed stones to drain the kidney via a tube and prevent backflow. complex cysts (rule out cancer). * 32yo man is seen for hypertension and hematuria. destructive bone disease (serum Ca level). * PKD diagnosed with renal ultrasound. ureter. -------------------------------------------------------------------------------------------------------------------------------------------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. What is the next step in the diagnostic evaluation? Answer is pregnancy test. also pancreas. open surgical removal is performed. Intracranial aneurysms (10%) berry aneurysms that can lead to subarachnoid hemorrhage. fat malabsorption (treat problem). * You should always try to determine the type of stone the patient has. * Treatment for increased calcium absorption (thiazides). dialysis/transplant for ESRD. It can be combined with lithotripsy. PTH level). * PKD is autosomal dominant in 90% of cases. impaired circulation due to distortion of renal vasculature leads to increased renin-angiotensin. If negative. So the patient will urinate at home into a funnel until a stone or particles are found. DO NOT DISTRIBUTE . Large or with significant obstruction requires surgical intervention. IVP (intravenous pyelogram) requires contrast. gene linkage studies are useful if considering kidney donation to affected relative. Small stones at the ureteropelvic junction (UPJ) almost always pass.5. * 35yo male has sudden onset of severe flank pain radiating to groin. ovaries. Renal failure occurs with progressive decline in function. control hypertension. * Initial tests in a “stone workup” include looking for increased calcium absorption (24h urine calcium). asymptomatic in childhood. * Ureteroscopy involves putting cystoscope through urethra up into bladder then fragments stones and pulls them out with forceps or baskets. For adults and children at risk. cysts not universally present until about 30s. infections. idiopathic hypercalciuria (thiazides). * PKD involves multiple renal cysts. with nausea and vomiting. identifies radio-opaque and even some radiolucent stones. struvite) or extensive anatomic abnormalities. greasy stools). pain may be constant or spasmodic. The absence of hematuria argues strongly against kidney stone. Is a homogenous cysts without echos (fluid filled sac). Stones and infection also occur. KUB (kidneys. * Spiral CT is the test of choice as it is fast. If pregnancy test is positive. vitamin C excess (discontinue vitamin C). Cause is uncertain. Sonogram is the test of choice for identifying stones in pregnant women. infancy). nausea and vomiting common.g. morphine) and high flow IVF. Mitral valve prolapse (25%). Urinalysis shows hematuria. * Extra-renal manifestation of PKD include hepatic cysts (50%). difficult to interpret as gas may be in the way. No treatment is needed unless large or symptomatic. Colon diverticula more often than in general population.30 - . only 2/3 have cysts in their teens. * Treatment of PKD is manage complications. * Genetic diagnosis can be done with prenatal amniocentesis and chorionic villus sampling (CVS). What is the best first test to support the diagnosis of kidney stone. * For complex stones (e. What is the most appropriate initial treatment? Answer is analgesics (e. usually single. simple cysts (incidental). * Lithotripsy (ESWL) can be used for small renal (<2. treat UTIs/stones. * Simple renal cysts are usually incidental findings on sonogram or CT. * Say the 26yo female is not pregnant and the spiral CT shows a small radiolucent stone in the ureter.g. most sensitive. stones. hyperparathyroidism (treat problem).5cm) and ureteral (<1. * PKD causes 5-10% of end stage renal disease needing dialysis. idiopathic hypercalciuria (24h urine calcium). screening of relatives at risk.

Hypertensive emergency is uncommon. * Treatment for hypertensive emergency is nitroprusside infusion. but also a small (2cm) cyst on left kidney with complex echos. renal failure is BUN/Cr. diabetics. * BP measurement method: patient resting quietly for 5 minutes. * Chronic complications include heart disease with >1million MIs per year. patient may present with heart attack or retinal hemorrhage. If BP systolic < 130 or diastolic < 85. By definition. blurred vision). and males > females. Cushing is remove pituitary adenoma. What is the next step in the evaluation. * Chronic complications include CVA (400. * After you get a first blood pressure reading. Hyperthyroidism can cause HTN (tremor. papilledema. * Essential hypertension has no clearly identified cause or reversible process. hyperthyroid is ultra-sensitive TSH.31 - . Sonogram to study gallbladder reveals gallstones. complex renal cysts are cancer until proven otherwise and need CT-guided needle biopsy. * Say the patient comes back and their HTN is confirmed. Renal artery stenosis is found by bruit on abdominal exam or sudden abrupt onset of HTN. then yearly. when do you have to get the patient back for a confirmation? If BP systolic > 180 or diastolic > 110. His history and exam are otherwise unremarkable. 400. Also nitroglycerine (with MI). Renal failure can be discovered by creatinine level elevation. < 5% of HTN is secondary. pheochromocytoma is VMA and metanephrines and catecholamines. renal artery stenosis is captopril renogram in young (fibromuscular) and Doppler flow in elderly (atherosclerotic). * 62yo man is being evaluated for RUQ abdominal pain. confirm on 2 subsequent visits. * So for secondary HTN causes. * Most common presentation is incidental finding in an asymptomatic individual. obese. or found during workup of hematuria or abdominal pain. * “White-coat” hypertension is thought to occur in about 20% of cases of diagnosed HTN. Coarctation of the aorta can be found by pulse lag. cerebral impairment (ischemia. creatinine. a complex cyst is cancer until proven otherwise. acute eye findings (hemorrhages. * Hypertensive emergencies need immediate treatment: angina or CHF. * What is the initial treatment if a secondary cause is suspected? Medication-induced is stop meds and follow BP. then 2 months. labetalol. * Ambulatory BP monitoring gives data for a 24h period. physical. goiter). potassium. Polycystic kidneys can be found by mass or hematuria. do history. polycystic kidney is renal sonogram. coarctation is ultrasound studies. CT scan confirms findings. seated with arm at heart level. useful for suspected “white coat” hypertension. hyperthyroid is beta-blockers and anti-thyroids. then 1 month. -------------------------------------------------------------------------------------------------------------------------------------------Hypertension (HTN) & Hypertensive Emergencies * Optimal is systolic < 120 and diastolic < 80. average of 2 readings. due to some other condition that is often reversible. and no hematuria. * Stage 1 hypertension is systolic 140-159 or diastolic 90-99. * High risk groups for HTN include African Americans. * Stage 2 hypertension is systolic 160-179 or diastolic 100-109. buffalo hump. * Investigating secondary causes can be done by history.g. Answer is cyst aspiration/puncture. severe headache). Normal is systolic < 130 and diastolic < 85. * 32yo previously normotensive man sees you for a work physical. renal failure (5. aldosteronism is aldosterone level. exam. Hyperaldosteronism will come with low potassium. coarctation is surgical. Must do a percutaneous aspiration biopsy (CT needle aspiration). * Hi-normal is systolic 130-139 or diastolic 85-89. and basic labs.Study Notes – Internal Medicine James Lamberg 28Jul2010 * Complex renal cysts are usually incidental findings on sonogram or CT. multiple (complex) echos/septations seen on CT or ultrasound. aortic regurgitation is echocardiogram. 60% of persons over age 65 have HTN and 75% are not controlled. regardless of size. bladder encircles 80% or more of arm. * Complex renal cysts vary in size. that is 1/4 of the adult population.000 ESRD/year). pulse striking earlier in radial than femoral arteries. Perform a physical exam and laboratory investigations to seek secondary causes.000 new CHF per year. subarachnoid hemorrhage. Aortic regurgitation has high systolic pressure and low diastolic pressure. * Epidemiology shows 50million Americans with HTN. then every other year. Cushing is dexamethasone suppression test and/or cortisol. Cushing disease will have striae. * Stage 3 hypertension is systolic 180+ or diastolic 110+. rounded moon-facies. What is the next step in evaluating his blood pressure? Answer is return in 1-2 months. If BP systolic 160-179 or diastolic 100-109. murmur. aldosteronism is DO NOT DISTRIBUTE .000 strokes/year). renal artery stenosis is angioplasty. If BP systolic 130-139 or diastolic 85-89. seasonal rhinitis spray). and seek/control atherosclerotic (ASHD) risks. Chronic complications can develop. polycystic kidney is ACE-I (maybe) and renal transplant. eye disease. * Again. If BP systolic 140-159 or diastolic 90-99. Pheochromocytoma presents with sympathetic episodes. BP is 170/99. * What is the best test if a secondary cause is suspected? Medication-induced is stop meds and follow BP. Medication causes include birth control pills and alpha-agonists (e. Patient has no symptoms from left kidney. enalapril. then 1 week. seek end-organ damage.

AAA (exam vs sono).32 - . recommended drugs: methyldopa is first line. cefazolin. Multiple BP readings over 2-3 months confirm hypertension. CHF due to systolic dysfunction. History is unremarkable except vague LUQ abdominal pain for past 6 months. Why don’t we use methicillin? Because it causes interstitial nephritis. Conrad Fischer. Re-consider secondary causes. homocysteine levels). * “Double-duty situations”: calcium-channel blocker for Raynaud. * What if you start treating a patient and the hypertension is not responding. stage 1 if it does not respond to lifestyle modification). folic acid. atrial fibrillation. aureus. patient may be confused about treatment regimen. SVT. clarithromycin. sedentary lifestyle. Urinalysis shows hematuria. but are not first choice. The antibiotics do however. most common cause of osteomyelitis is S. * Risk factors for atherosclerotic heart disease (ASHD) are smoking. MD -------------------------------------------------------------------------------------------------------------------------------------------The organisms that cause certain diseases do not change over the years. ACE-I will improve renal blood flow a bit and lower risk of progressive renal damage.Study Notes – Internal Medicine James Lamberg 28Jul2010 remove aldosterone tumor. but should be reserved for methicillin-resistant staph aureus (MRSA). For lifethreatening penicillin allergies. exam shows LUQ fullness. DO NOT DISTRIBUTE . then we should avoid all the beta-lactam antibiotics. gram negative rods. aortic regurgitation is ACE-I and valve replacement. no evidence it improves heart disease. * Medications are first-line for uncomplicated essential hypertension (stage 3. Alpha blocker for prostatic hypertrophy. naf. -------------------------------------------------------------------------------------------------------------------------------------------Kaplan Videos (2001) – Infectious Disease with Dr. * Hypertension in pregnancy. Clue to this palpable artery with inflated cuff. or recent MI. choice for life-threatening penicillin allergy. * Ampicillin. you will find there was beta-lactamase in the staphylococcus. that causes a little rash. just superior in its resistance pattern. nafcillin (not methicillin). Other labs are normal including creatinine. salt reduction. diabetes. vitamin B12. C-reactive protein level also not proven to be linked to heart disease. Beta-blocker for migraine headache. so don’t worry if the allergy is a little rash. most stage 2. what do you use? Not methicillin. coli. * Another alternative for staphylococcus and streptococcus (e. * Special circumstances: ACE-I used in diabetes. cephadroxil. Contraindicated drugs include ACE-I and angiotensin receptor blockers (ARBs). and laryngeal edema so they had to get intubated. and hypotension. 5% cross-reaction with penicillins at most and almost never anaphylaxis. then dopamine drip in the ICU. teratogenic. newer risk factors (C-reactive protein. and stridor. Physical exam and all lab tests are unremarkable. -------------------------------------------------------------------------------------------------------------------------------------------Overview of Antibiotic Therapy * Most common cause of pyelonephritis is E. ECG (vs echo vs nothing) for left ventricular hypertrophy. amoxicillin alone is good for streptococcus. diclox. mild renal insufficiency. otherwise no ASHD risk factors. dicloxacillin. Most common cause is noncompliance. lower extremity pulses. penicillin allergy) is a beta-lactam drug. renal failure is renal transplant. pheochromocytoma is alpha-blockade and surgery. is artery calcification that prevents full compression of the artery by the blood pressure cuff. usually in elderly. * Homocysteine levels can be lowered with vitamin B6. hyperlipidemia. Diuretics (thiazides) are first or beta-blockers. Consider alcohol abuse and NSAIDs. What is the best initial step in his treatment? Answer is smoking cessation. Macrolides with clindamycin will cover staph/strep. carotid bruits. firstgeneration cephalosporins like cephalexin. penicillin. * What if patient says they have a penicillin allergy. Use ox. cloxacillin. clox. * Hypertension treatment initially for stage 1 and maybe stage 2 is lifestyle modification: weight reduction. azithromycin. * So what antibiotics go along with staph/strep. but being investigated. and anaerobes? * If you do PCR resting on Egyptian mummies from 5 thousand years ago. * Osler phenomenon. * End-organ damage can be investigated by looking for retinopathy. * 45yo previously normotensive man sees you for work physical and BP is 170/99. * Antibiotics for staphylococcus and streptococcus are oxacillin. * 45yo previously normotensive man sees you for work physical and BP 165/92. * With methicillin-sensitive staphylococcus. possibly alcohol reduction is in large amounts. History reveals 1PPD smoker for 30 years. but not for staphylococcus. possibly better than beta-blockers in African American population if adding to diuretic. exercise. Labetalol or hydralazine also acceptable. * Calcium-channel blocker used in isolated systolic hypertension in elderly.g. obesity. thus giving a falsely high reading. smoking cessation. then got IV steroids. CHF. What is the most appropriate test for a secondary cause of hypertension? Answer is renal ultrasound to rule out polycystic kidney. Vancomycin not superior in efficacy to ox/clox/diclox/naf. Multiple BP readings over 2-3 months confirm hypertension. * Macrolides: erythromycin. Vancomycin works.

tobramycin. So what will tell you right now what type of organism you have? Answer is cell count. -------------------------------------------------------------------------------------------------------------------------------------------Meningitis * 57yo man comes to the ED with fever and a headache. enterobacter. * The most common neurologic problem after meningitis is deftness. Gram-stain is 50-60% sensitive. meropenem). rickettsia. very sensitive and specific. * With papilledema you worry about herniation. facial nerve palsy).” because you cannot determine focality. headache. DO NOT DISTRIBUTE . an LP would not cause herniation. ‘that’s not my prostate.33 - . what is the most accurate diagnostic test? Answer is culture. it can happen within hours. expect HIV patient with < 50 CD4 T-cell count. * Cephalosporins range from strong Gram-positive coverage at first-generation (poor Gram-negative) to strong Gram-negative coverage at third-generation (poor Gram-positive). All other tests are compared to culture. aminoglycosides (gentamycin. third-generation cephalosporins (ceftazidime. implying meningitis. fluoroquinolones (ciprofloxacin. * CSF analysis: Which form of meningitis can give an elevated protein and decreased glucose in the LP? Answer is all. amikacin). India Ink is about 50% sensitivity (good if positive. * Antibiotics for anaerobes are metronidazole (particularly good for abdominal). so they cover Gram-positives and Gram-negatives. and focal findings. right? We just get some IgM acutely and IgG chronically. Best initial test? Answer is not India Ink. * Rocky Mountain Spotted Fever (RMSF) is not seen on Gram stain because it is intracellular (rickettsia). culture negative. or syphilis on Gram stain. extended spectrum penicillins (piperacillin. trovafloxacin. Gram stain negative. Amphotericin B (better than fluconazole for saving life in meningitis). Other information from the LP can help tell you the diagnosis. Should you start this patient with fluconazole? No. gatifloxacin. Patient also needs to be able to follow commands. CN VIII damage. ceftriaxone). you should start the patient on antibiotics first (dose of ceftriaxone). strep pneumonia. “You go to do a rectal later and say ‘my that’s a smooth prostate’ and the patient says. moxifloxacin). * So 57yo man has fever. Lyme also not seen on Gram stain because it is a spirochete. What if they want you to know it’s a brain abscess? Fever. second-generation cephalosporins (will not cover pseudomonas). * Carbapenems cover Gram-negative and Gram-positive. * So. pseudomonas. don’t jump to imipenem. Photophobia or seizures or nausea or vomiting are too nonspecific here. Remember the Weil-Felix test? Forget it. use doxycycline instead. However. headache. streptomycin.” * TMP-SMX is only good for uncomplicated cystitis and prophylaxis against pneumocystis pneumonia. but you should not use them for Gram-positive infections (like strep throat) because there are better drugs exclusively for Gram-positives. that’s my pons.’” * When you have infectious diseases. When do you wait for results of the culture? Never. but you’d rather be alive with a clean LP than dead with an accurate LP. so won’t be positive most of the time. citrobacter. So this is very easy. Now what? Answer is serologic testing to look for specific antibody against Lyme and RMSF. levofloxacin. coli. positive in 95-98%. * Antibiotics for Gram-negative rods are aztreonam. viral. Doxycycline used for Lyme (mild disease: rash. * Chloramphenicol is never the right answer. neomycin. no other use. If you see 1000s of polys. Fourth-generation cephalosporins (cefepime) are a combination of first-generation and third-generation. “Do not swat a fly on your friend’s head with a hammer. Legionella. What about encephalitis? Fever. altered mental status (confusion. where others give 10-100s of lymphocytes. tuberculosis. Fluconazole is continued life-long. * CSF cell count: Only bacterial gives you 1000s of polys. Chlamydia. give ceftriaxone. then follow up with fluconazole forever. What about 10-100s of lymphocytes? Could be fungal (cryptococcus). You also can’t see TB. encephalopathy). it causes aplastic anemia and Gray Baby Syndrome. What is the first test? Do you do a lumbar puncture or a CT scan? What is the first test? Lumbar puncture (LP). sparfloxacin. If you had a mass lesion that was so small it did not cause focality. means nothing if negative). azlocillin. such as “squeeze my hands. stiff neck. carbapenems (imipenem. mezlocillin). Lyme disease. ticarcillin. syphilis. * For cryptococcus meningitis. headache. Answer is cryptococcal antigen testing. * Nitrofurantoin used for UTI in pregnancy. klebsiella. * If you are going to do a CT prior to the LP. use amphotericin B. Only do a CT scan prior to a spinal tap if papilledema or focal findings that would imply a brain mass/abscess. Which gives it most often? Bacterial. Doesn’t that ruin the sensitivity of the LP culture? Yes. clindamycin (does not cover bowel well). carbapenems as well. as these are intracellular organisms. Rocky Mountain Spotted Fever.Study Notes – Internal Medicine James Lamberg 28Jul2010 * Gram negative rods include E. This helps you determine if you should use doxycycline or ceftriaxone. * Tetracycline is not the correct choice anymore. else cryptococcal meningitis recurs. A specific additional symptom to lead you down the right path would be stiff neck (nuchal rigidity). proteus. CSF from lumbar puncture shows 10-100s of lymphocytes. If you have an exclusively anaerobic infection. viral meningitis.

Lots of encephalitis in the world. cefixime. TB culture. Then do a biopsy. toxoplasmosis. Next step is brain biopsy. we have a lesion with mass effect giving focal findings.” Or you radiate the patient for 6 weeks and they say. cefaclor would work. Some mild benefit possibly with steroids given prior to starting antibiotics and LP. resistance) the efficacy of amoxicillin is just as good as any of the other antibiotics. assume toxoplasmosis and give pyrimethamine and sulfadiazine for a couple of weeks and repeat CT scan.” You have to biopsy to know. nifty idea but not necessary. Massachusetts. Amoxicillin/clavulanic acid works too. You don’t want to start antibiotics and have the patient come back with a permanent deficit saying. neutrophil and T-cell defects. This isn’t fungal because there are polys present. Two groups of diseases that give ring-enhancing lesions are cancers and infections. Bolivian hemorrhagic fever. culture negative). which has largely replaced the biopsy. 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. * Treatment of herpes encephalitis is acyclovir. oligodendroglioma. and confusion (encephalopathy). Macrolides azithromycin. You may see a red bulging tympanic membrane. If not child. * Lumbar puncture should come with PCR. if you haven’t recently been treated (i. Staph. steroids (neutrophil and T-cell defect). Head CT will show ring. diagnose with TB stain and AFB cultures. Do a CT to see ring-enhancing lesion. * So again. What is the next step? Head CT. * When do you answer steroids for meningitis in adults? Answer is TB meningitis. target rash (erythema migrans) and outdoor activity. -------------------------------------------------------------------------------------------------------------------------------------------Encephalitis * Fever. -------------------------------------------------------------------------------------------------------------------------------------------Brain Abscess * Fever. much broader range of disease. Lyme in Connecticut. The head CT will most likely be normal. New Jersey (North East). Colorado tick fever. has a lumbar puncture with elevated protein and decreased glucose. * When do you answer intrathecal antibiotics? Answer is never. the only way to know what it is. AFB (acid-fast bacillus) stain and culture. because listeria is resistant to all forms of cephalosporins. headache. cryptococcal antigen testing. * Second and third generation cephalosporins. pyrazinamide. eastern equine encephalitis. INH. centripetal (moves centrally) rash and outdoor activity. diagnosis is by exclusion of the others. astrocytoma. Answer for management is give ceftriaxone and ampicillin. based on American Society of Otolaryngology. RMSF. Venezuelan hemorrhagic fever. there is no treatment. If Lyme. not necessary. * Next step depends on HIV status. What is suggestive of herpes on a lumbar puncture? Answer is increased red cells. leukemia/lymphoma elderly or neonate then do empiric coverage. on steroids for CLL.e. If the case is clearly encephalitis and they ask diagnosis. your best bet is to answer herpes. western equine encephalitis. pain on pulling pinna. anaerobes. “doc. ethambutol. You have to suspect the specific disease. do a biopsy to see what is at the ring-enhancing site. clarithromycin work. “doc. If TB. Kentucky.Study Notes – Internal Medicine James Lamberg 28Jul2010 * So are with “atypical” results (Gram stain negative. and focal findings. plus clear CT scan favors against subarachnoid. Do not do LP. * Elderly neonate is HIV positive. new fluoroquinolones like levofloxacin. Next step is CT scan (or MRI). I heard antibiotics don’t work well for glioblastoma. This patient is immunocompromised. If patient is HIV positive. the radiation isn’t working for my staph aureus. are we just going to order Lyme. Congo Crimean fever. Intrathecal antibiotics is like intra-cardiac epinephrine. gatifloxacin work as they cover strep pneumonia. Next step is not lumbar puncture because the patient will herniate and die. * If you add all those cause of encephalitis and multiply by ten. -------------------------------------------------------------------------------------------------------------------------------------------Otitis Media & Sinusitis * What is the most sensitive physical finding for otitis media? Answer is immobile tympanic membrane on insufflation. look for the centripetal rash. it shouldn’t matter. If viral.34 - . Carolina. occasionally fever. 90% of the time it is toxoplasmosis or lymphoma. cefuroxime. mildly hemorrhagic. * Test TB (meningitis and pulmonary) with TB stain. Methotrexate is given intrathecal in ALL (acute lymphoblastic leukemia). rifampin. viral serologic testing. * Things that put you are risk for listeria include immunocompromised. moxifloxacin. headache. RMSF in Alabama. 3200 polys. HIV (T-cell defect). * If patient is HIV negative. How do you know it is not a subarachnoid hemorrhage? There will also be increased WBCs from infection.or contrastenhancing lesions. If the CT scan is the same. they still are not as common as herpes encephalitis. Tennessee. strep. glioblastoma. Gram stain negative. New York. half the time the otitis media resolves on its own because they are viruses. In HIV. viral encephalitis. * Treatment is amoxicillin. So what organism do we have to cover? Answer is listeria. * If RMSF. DO NOT DISTRIBUTE . syphilis serology with a VDRL and FTA on all of them? Nope.

* The best initial diagnostic test is an x-ray. * What is the most accurate diagnostic test for this sinusitis patient? Answer is culture. azithromycin. strep. What is the next step in management. * Pseudomonas pneumonia seen in the ICU in intubated patients. first for respiratory infections. * If patient is allergic to penicillin. then this is bronchitis. gatifloxacin. Many people will not think about ordering this type of test unless they know it exists. influenza. 30% h. Clarithromycin) or quinolone. Look at IgG and IgM serology. legionella. tooth pain. * Lobar infiltrates is regular bacterial pneumonia. it doesn’t seem logical unless you understand the test. What test should you order first? Answer is x-ray. you will not see the diagnosis. cough. consolidations). abdominal pain. most common is strep pneumonia. you don’t get the diagnosis half the time. Look for a patient with GI and CNS problems. Azithromycin. hospital acquired infection. * Why is sputum stain not first? Even when you do the culture. poor dentition. * When do you wait for the results of culture? Answer is never. so not a good way to make a diagnosis. Elderly patient with lobar pneumonia and has COPD or smokes often. rhinorrhea. pneumonia. * Why don’t we Gram stain the vagina? Gardnerella is normal flora. looking for the surface antigens of strep pyogenes. If CXR is normal (no infiltrates. Ampicillin would work also. viral pneumonia. chlamydia. clarithromycin.” Mycoplasma not seen on Gram stain (no cell wall) and not grown in regular culture. DO NOT DISTRIBUTE . Most accurate test is Gram stain. then it is strep pneumonia. sinus tenderness. A patient presents with lots of coughing and you’re getting a urine test. Atypical means it is not seen on a Gram stain and not grown in regular culture. Why do you not do a Gram stain for pharyngitis? It will not tell you if you have strep pyogenes. “walking pneumonia. intoxicated. it can’t tell you what type of strep is there. patient. Doxycycline also works. moxifloxacin. Elderly patient with lobar pneumonia is pneumococcus. so we need clue cells to see when there is too much. effusions. All you know is this is a respiratory infection. adenopathy. loss of gag reflex. moxifloxacin. decreased transillumination of sinuses. * How do we determine the types of pneumonia if infiltrates are found on CXR? There will be lobar infiltrates or bilateral interstitial infiltrates. If bilateral interstitial infiltrates. * In long-term alcoholics with lobar pneumonia. * 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. you increased your risk of aspiration. * What is the best diagnostic test? Answer is biopsy/aspiration. clarithromycin. * Why don’t we Gram stain or culture sputum for an abscess? Everyone has anaerobes in their sputum. and exudate. * Intubation aspiration. To get an abscess. pneumocystis pneumonia. Get culture and start antibiotics. Urinary antigen for legionella is 99% sensitive and specific. You can’t say this is influenza. klebsiella. Pen VK. could be mycoplasma. most common is strep pneumonia. Test for legionella pneumonia (diagnosis) is urine antigen. For below the diaphragm we use metronidazole. * Patient has bilateral interstitial infiltrates. diarrhea. * Acute otitis media (AOM) is about 40% strep pneumonia. We Gram stain sputum because strep pneumonia with lancet-shaped diplococci are not normal flora in the mouth. confusion. -------------------------------------------------------------------------------------------------------------------------------------------Pharyngitis * Symptoms are sore throat. In smokers and COPD patients with lobar pneumonia. If you don’t screen for it with the test. * Treatment for bronchitis (with sputum) is second or third cephalosporins. azithromycin. Answer is give amoxicillin. healthy. but not first. 20% moraxella catarrhalis. * The rapid strep tests are latex agglutination tests. hemophilus. stroke. influenza most likely to be seen in smokers and COPD patients (but not most common). Cold agglutinin testing for mycoplasma is not sensitive or specific enough. Klebsiella pneumonia is more likely to be seen in alcoholics (but not most common). * Erythromycin has an advantage over the others as it can prevent rheumatic fever. * Young healthy person admitted for lobar pneumonia is pneumococcus. bronchitis. It accounts for about 5-10% of community acquired pneumonia. levofloxacin. -------------------------------------------------------------------------------------------------------------------------------------------Bronchitis & Pneumonia * Fever. * Mycoplasma pneumonia usually seen in young. H. A CT is more accurate than an x-ray. We do Gram stain the cervix to look for neisseria gonorrhea. the patient must have an increased risk for aspiration and an oral infection.Study Notes – Internal Medicine James Lamberg 28Jul2010 * 28yo female with headache. * For anaerobes above the diaphragm we use clindamycin. gatifloxacin. staph. levofloxacin.35 - . * Treatment for mycoplasma or legionella is macrolide (Erythromycin. with or without sputum. Answer for treatment is oral penicillin. what do we use for pharyngitis? Second or third generation cephalosporins. * How do we know if the patient has an abscess? Halitosis due to anaerobes.

night sweats. weight loss. Steroids will increase the inflammation and thus increase the ability to transfer oxygen across the interstitial membrane. PPD is used for screening the asymptomatic. What is the next best step? Answer is treatment. ethambutol. * With pneumocystis pneumonia. What do you do for this patient? Answer is nothing in asymptomatic hyperuricemia. What about 20mm of erythema? No. short-course steroids for 2-3 weeks will not hurt. Anything in the brain can also cause SIADH. Sorry. * What effect does BCG (Bacillus Calmette-Guérin vaccine) have on these recommendations? None. Treatment is doxycycline. never develop TB. optic neuritis. that’s for sick people. cough. Presenting symptom is usually dyspnea. has cough. There are over 2 million in prison in the U.Study Notes – Internal Medicine James Lamberg 28Jul2010 * Most specific test for legionella is buffered charcoal yeast extract agar (BCYE). Antibody testing also takes weeks and is never available to make a treatment decision. How much risk do you have of developing the disease? Answer is 10% in a lifetime. CXR is negative. You put the patient in isolation. * On hospital day 2. Now. Up to 60% of prisoners are PPD positive (tuberculosis). PO2 is 65. but it takes a couple of weeks. What if the mummy had BCG? 9 months of INH. asymptomatic. * If your PPD is positive. what is the next best step? Answer is sputum. What about a 3. Also. at any time. What about 2 meters of erythema? Nope. for screening populations at risk. * What is a positive PPD? 10mm of induration. due to ventilation and crowds that you get there. but isn’t it better than dying of hypoxemia today? You’d rather be alive with re-activated TB then dead with no TB. Serology diagnoses Q-fever (coxiella burnetii). this HIV patient develops the most common side-effect of IV TMP-SMX. not PPD skin test. Except in HIV. Anything in the lung can cause SIADH. where it is 10% per year. Patient has fever. -------------------------------------------------------------------------------------------------------------------------------------------Tuberculosis (TB) * 37yo male prisoner at maximum security prison. * Tuberculosis is essentially an economic disease.. what does this mean? It means you have been exposed. What is the next best step in the management of this patient? Answer is oxygen. The amount of TB in a country is proportional to the amount spent on public health. Neuropathy. DO NOT DISTRIBUTE . organ transplant recipients. You check sputum because PPD is not to diagnose acutely ill patients. For prophylaxis. * Ethambutol affects what organ? Eye. Without that history.. * 71yo woman who has never been tested. rifampin (RIF). close contacts. INH causes increased urinary loss of vitamin B6. What is the next step in management. Pentamidine is only second-line if patient has IV therapy. Sniffing a sheep (Yemenite sheep) placenta. iNh. the second-line is dapsone.S. * Neuropathy occurs with isoniazid. A interferongamma quantification test (QuantiFERON-TB) may be used. Severe is PO2 < 70. That means 90% of people who are PPD positive. * Which TB drug causes hyperuricemia? Pyrazinamide. How many drugs should patient’s be started on? 4: isoniazid (INH). What is the next best step in the management of this patient. Answer is 9 months of INH. * PPD is 5mm induration in HIV. steroid use. What about 10mm of erythema? No. It shows an apical cavity and infiltrate. then give TMP-SMX (co-trimoxazole). Induration is the only important point. the coxiella aerosolizes at the time of birth and they get the pneumonia. No symptoms. * Say sputum is positive for AFB (acid-fast bacteria) stain. CXR shows bilateral interstitial infiltrates. But there is no IV dapsone. That side-effect is a diffuse maculopapular hypersensitivity rash. BCG will not give you 10mm of reactivity. patient is HIV positive with < 200 T-cells. * 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.” * Any cause of pneumonia can cause hyponatremia. and the incidence will rise. Coxiella is the only airborne rickettsia. “Hmm. * Patient has bilateral infiltrates after sniffing a placenta. What? If I’m from India I don’t want to eat isoniazid for 9 months. Ethambutol. That means 10 people will get isoniazid for 9 months to prevent that one single case. Except 5mm induration in HIV positive patients because immune system cannot make it to 10mm. sputum. * Abnormal red color with all your body fluids with rifampin. PPD is 16mm. Eye. Red. How what do you put the patient on? Answer is pentamidine. You would need the animal exposure history. But isn’t it dangerous to give steroids to someone who is immunocompromised? Maybe. they’ll test everyone. it doesn’t matter no matter how much you think it does. * Steroids used if hypoxemia is severe.36 - . What is the major side-effects of IV pentamidine? Answer is pancreas problems. pyrazinamide (PZA). found to be PPD positive.791yo Egyptian mummy. ever since this new guy came to town everyone is getting Gonorrhea. Answer is CXR. * Which TB drug cause hepatotoxicity? Answer is all of them. So people around animals at the time or birth. not me. You give 4 drugs because of the possibility of resistance. Rifampin. People will be like. negative CXR? What do you do? 9 months of INH. you can’t figure it out.

37 - . not protozoal (crypto. watery. * Protozoans. not in an individual patient. This patient got her diarrhea from what she had from dinner the night before or what she had for lunch the day before. she has a big. * If the patient is asymptomatic and you get a positive PPD. Legionella and air conditioners. Not HIV. salmonella/shigella and campylobacter is 24-36 hours.S. Yes the travelers and undercooked red meat. HepE in the East (SE Asia. because you have to wait for the culture results. Cambodia. you give the 4 drugs. the last thing you ate is not necessarily the thing that gave you diarrhea. Yersinia. * When you compare risk factors with individual presentation. febrile. Treatment is anti-histamines. D. you just caught early reactivation of TB. get transaminitis. fatigue. giardia). light stool (bilirubin not in stool anymore). tiredness. you do a CXR. it depends on what you eat. If sputum shows TB. -------------------------------------------------------------------------------------------------------------------------------------------Infectious Diarrhea * 27yo female medical student has a lunch today at 3pm. INH. Hepatitis B. Hepatitis G “is a virus with an identity crisis. Your decision point with diarrhea and food-poisoning is blood or no blood. you look for ova and parasites in the stool. with a temp of 102 and abdominal pain. G. HIV associated diarrhea is cryptosporidium and there is no therapy and there isn’t going to be a therapy. salmonella. If positive. you get increased ALT. At 6pm. use ciprofloxacin. This also is associated with wheezing and a rash. just normal people. Isn’t erythromycin better for campylobacter? Yes. but you don’t know if it’s campylobacter. not IV drug users. and D through blood. What is the cause of her diarrhea? Not staph aureus. sex. like vomiting. * If you are given no history and bloody diarrhea. perinatal. campylobacter is statistically the most likely. * Giardia associated with camping and homosexual men. you get INH for 9 months. not bacillus cereus. Vietnam.S. septic. poopy. -------------------------------------------------------------------------------------------------------------------------------------------Hepatitis * Hepatitis A. Treatment is metronidazole. HUS. few cases. For salmonella. Can you get hepatitis A sexually? Well. Why not culture? It is difficult to culture. mahi-mahi. but that is after you’ve already diagnosed it and you did an outbreak investigation. The only way to distinguish the cause of bloody diarrhea is by culture. A patient is found to test positive for hepatitis G after a blood donation. shigella. It could be campylobacter. Shellfish association is Vibrio parahaemolyticus. not shigella. Yea. People who living in Wyoming (100% sensitivity to TB medications. HUS is a rare and uncommon association. * Also. dark urine (bilirubin in urine). * Summary: individual presentation of the patient matters the most. tuna. you check the sputum to make sure you’re not dealing with active TB. not homeless. for basic science we learned staph aureus and bacillus cereus is 2-6 hours. If CXR is negative. C. not E. Risk factors do not matter if the patient has blood per rectum and a fever. not healthcare workers. DO NOT DISTRIBUTE . smelly. * What if you do not get blood in the history? Check leukocytes. * Which form of food poisoning (diarrhea) causes symptoms the earliest after ingestion? Answer is scombroid. RIF. yea after you’ve diagnosed it and we culture all the air-conditioning systems. * Hepatitis A transferred via food and water (fecal-oral). the most important is individual presentation. Laos). difficile associated with antibiotics.Study Notes – Internal Medicine James Lamberg 28Jul2010 * Interferon gamma testing is not affected by BCG at all. clostridium perfringens is 12 hours. you give INH for 9 months. increased bilirubin. HepA is most common in the U. weight loss (turns off appetite). Yes. like hypotension. protozoa. ethambutol (EMB). Most likely cause is campylobacter. not vancomycin. coli. C. cereus. but you need to know it. Chinese rice. The fish eats organisms that make histamine in the flesh. splenomegaly. Campylobacter is the most common cause of invasive diarrhea in the U. B. most of the time it does not cause blood. what should you tell the patient to expect? Answer is nothing. This patient has blood in their stool. E. but not when the patient is walking in. always sensitive). staph and B. There was a hepatitis F for a little while. WBCs. E. coli will be associated with thrombocytopenia.” It doesn’t make you turn yellow. C. Viral is often seen in children. not any form of disease. renal failure. If sputum is negative. lose weight. not salmonella. cereus cause symptoms in 2-6 hours. hepatomegaly. * If PPD is positive. diarrhea. but they predominately present with upper GI symptoms. Test is via toxin. not viral. but patient has no antibiotics in the history. * C. through food and water. make dark urine. association is poultry. * With acute hepatitis. Hepatitis E (enteric) through food and water. or make light stool. B. coli. * Who gets the 15mm cutoff for PPD testing? People who should have never been tested in the first place. malaise. bloody. but they found it was C. Hepatitis G does not cause clinical disease. difficile can give you blood. It could not be viral. PZA. staph. That is why it is named difficile (Spanish for difficult). * When you have to treat the non-blood diarrhea causes. You treat if they have very severe disease. then white cells or no white cells. sardines. E. Treatment is metronidazole first. It is from spoiled/rotten fish. Yes.

painless and firm ulcer. Hepatitis B is the only with surface antibody. ducreyi and with serology for LGV. * Syphilis chancre is painless and firm/indurated. * In real inflammation. strep. pleomorphic Gram-negative bacillus. an HIV retroviral. Presentation seen in syphilis chancre. D. Ribavirin/interferon can help prevent the most common cause of liver transplantation in the United States.S. otitis. Decision point is painful versus non-painful. If the vesicles become unroofed. cervicitis. * Acute or chronic is determined by the surface antigen being present beyond six months. ducreyi. Lamivudine. * What is patient is allergic to penicillin? Answer for primary/secondary syphilis is doxycycline. because it has greater sensitivity for primary syphilis. chancroid. Same for cervicitis. -------------------------------------------------------------------------------------------------------------------------------------------Sexually Transmitted Diseases * Patient presents saying their penis is burning. * Chronic HepC is treated with interferon and (and) ribavirin. IgG chronically. Stain. * Treatment for acute hepatitis is nothing. core antibody. but about 1 year in HIV patients. this differentiates urethritis. Ask if there is discharge. What is the next best step in the management of this patient? Answer is treat herpes simplex with acyclovir. meaning they get rubbed and the top comes off showing an ulcer. * Treatment is ceftriaxone (for gonorrhea) and azithromycin (for chlamydia). How do you distinguish via history and physical exam which type of hepatitis we have? You can’t. something like cancer would be carcinoid. treat. like meningitis. What are you going to ask. culture. pancreas) there are 4-5 people waiting. * 27yo man has adenopathy. * Mycobacterium avium prophylaxis with a single weekly dose of azithromycin. * 27yo man comes to clinic with multiple small painful genital fluid-filled vesicles. IgM acutely. is lung cancer. culture. Once you get to secondary syphilis. but you do need to know route of administration. C. hemophilus. * Chronic HepE does not exist. so serology with just positive sAb is vaccinated. staph. try to look for Gram-negative diplococci. bronchitis. VDRL and RPR are at 100% sensitivity. even an aminoglycoside.S. just so you cover both gonorrhea and chlamydia. * Syphilis is rarely seen in our population. DO NOT DISTRIBUTE . You won’t find a dark field scope anywhere. treatment is IV penicillin. If discharge. However. Chronic HepA is treated with nothing. “-oid” means similar. urethritis. covers chancroid. have you had sex with any yellow people recently? There are 5 types of hepatitis with 2 transmission methods and 1 presentation. You have to have the time-course with it. looking for cellular atypia. combined with ribavirin is 40-50% cure rate. * Azithromycin is fantastic. treatment is IM penicillin. VDRL? Only about 75% sensitivity with VDRL and RPR in primary syphilis because it needs time to make an antibody response. * Chancroid is painful. so you do the RPR/VDRL then FTA. Lamivudine is an oral pill to prevent the most common cause of cancer death in the world. * Chronic HepB is treated with interferon or (or) lamivudine. * Neurosyphilis takes about 10 years to develop. In tertiary syphilis. and lymphogranuloma venereum (LGV). * If you are positive for surface antigen (sAg). anything will pass through the BBB. HepC is the most common reason for needing a liver transplant in the U. Chronic HepD is treated the same as HepB because you have to have HepB to get D. Treat with doxycycline. how long was your asymptomatic incubation period. Most common in U. Most common cause of cancer death in the world is hepatocellular carcinoma. lung. liver. so you do not need to Tzanck prep. * You do not need to know dose. MAC. or valacyclovir. * Desensitize and treat with penicillin in pregnancy as well. sinusitis. something like leukemia would be leukemoid. Do serology. famciclovir. core antigen. * Diagnosis is via anti-hepatitis A. surface antigen. doxycycline will not cross the BBB very well. you are infectious. gets rid of HepB sAg. Lots of treatments available. Interferon alone is 5-15% cure rate. Tzanck smear involves swab and putting on slide. and treat. initial test is a dark field. H. has urinary frequency. E serology. * Vaccination against HepB gives you surface antibody only. Treatment could be ciprofloxacin (for gonorrhea) and doxycycline (for chlamydia). so treatment is desensitize and treat with penicillin. What is the next step? Is it RPR. The FTA-ABS does not go away. * LGV is big beefed-up matted up lymph nodes. * 27yo man comes to clinic with genital ulcer and adenopathy. * Core antigen could be positive or negative. chlamydia. then you do a Tzanck and culture with Gram-stain for H. In tertiary syphilis. chancroid is painful and soft. Tertiary syphilis. That means you cannot tell just from the serology. * Primary and secondary syphilis. there is no chronic HepA. you lose some sensitivity because you start to lose antibody over time. You see the genital vesicles. swab.38 - .Study Notes – Internal Medicine James Lamberg 28Jul2010 * Patient presents and is yellow. try to find intracellular Gonorrhea. ulcers around them. For every organ that becomes available (heart. Testing can be done with Gram stain and culture. * It helps memory to think about what this actually means. Answer for treatment is single dose azithromycin. Next step is swab. and e antigen. it doesn’t determine if HepB is chronic. How do we tell if it is urethritis or cystitis. herpes (HSV). or any combination.

-------------------------------------------------------------------------------------------------------------------------------------------Skin Infections * Scabies. -------------------------------------------------------------------------------------------------------------------------------------------Medication Side-Effects * Interferon major adverse effect is flu-like symptoms. or other anatomic complication. We found hydralazine wasn’t as good as ACE inhibitors. Now we know dig is lousy and does not decrease mortality. dig. just pick what covers Gram-negatives. nafcillin.Study Notes – Internal Medicine James Lamberg 28Jul2010 * Patient has genital warts (condyloma acuminata). 7 days is for stones. GI symptoms (nausea. depression. Fever can help a little too because there is a little fever in cystitis and big fever in pyelonephritis. * Interferon causes aches. * What is the most superficial of all the bacterial skin infections involving just the epidermis? Weeping. Treatment is remove. Best initial diagnostic test for both is urinalysis. piperacillin. Answer is erysipelas. Most important thing to look for is WBCs. vomiting). You get the same symptoms with the flu. Staph here is staph aureus (not staph epidermidis). Cystitis is such a routine problem that there is a standard length of therapy. pregnant. Molluscum contagiosum gives warts with an umbilicated center. you can’t Gram stain an ultrasound. strep pyogenes. Now what is the next step? Ultrasound or CT or MRI and you find an abscess around the kidney. There is no specific drug. Why do board exams emphasize adverse effects? Say we’re in 1970. -------------------------------------------------------------------------------------------------------------------------------------------Cystitis & Pyelonephritis * 39yo women with urinary burning. what do you use? Answer is oxacillin. swab. crabs if genital) is found near hair areas. stain.g. * Which skin infection involves the dermis and subcutaneous tissues? Answer is cellulitis. * Which skin infection involves the epidermis and extends into the dermis? Causes swelling in dermal lymphatic channels and bright-red skin. Treatment is lindane or permethrin cream. dysuria. tumors. treatment is to drain the abscess. just remove it. Diagnostic test is scraping. vancomycin or macrolides. What is the most common side-effect of digoxin. strictures. * Best diagnostic test for cystitis and pyelonephritis is a culture. chop. So. You use the ultrasound because you know the patient has pyelonephritis and want to see what the cause is. Test is visual identification of wart. cut. * Do you have to drain the abscess or can you treat with antibiotics? Most of the time you drain abscesses. * If you’re not sure what type of skin infection this is. The strep in these skin infections is group A beta-hemolytic strep. Poxvirus gives small little warts. treatment of CHF would be digoxin and diuretic. Usually length of treatment is a matter of local tribal customs. tumor. It does not get to the dermal-epidermal junction so it cannot cause oozing above skin. Imiquimod is a local immunostimulant and the only treatment that does not go too far and burn the skin (e. urgency. Lice (pediculosis. 5 times smaller than lice. You can’t get rheumatic fever from this. pains. freeze (cryo). The most accurate test for abscess biopsy or aspirate. 3 days for uncomplicated.39 - . You can tell these apart by the pain. melt. So care was ACE-I. you can’t get sensitivity on an MRI. In 1985 for a short time we used hydralazine and nitrates. The problem is this happened while you were on antibiotics. Staph epidermidis lives on your skin and therefore does not cause infections of the skin. He’s digging and pooping. sarcoptes scabeii. Cough with ACE-I. If you have a mild penicillin allergy then use first-generation cephalosporin. you won’t have to edit questions much in the future. cloxacillin. ticarcillin. burn. Answer is impetigo. That could be aminoglycosides. Diagnostic test for warts not smear. diuretics. pregnant patients. That is interferon in your body. caused by strep. the adverse effects will not change. If lifethreatening penicillin allergy. because you make interferon yourself. No matter what the standard of care is. It stimulates the T-cells to react to the wart as foreign and sloughs it off. hydronephrosis)? * Say you put patient on antibiotics and 3 days later they are still sick. So if you’re writing board questions and you choose side effects to ask about. Bacteria in the urine is only significant in one patient population. fluoroquinolones. * Pyelonephritis is a drug that covers Gram-negatives. biopsy. honey-colored crusting of skin because it lifts up the epidermis. staph and strep. irritability. dicloxacillin. diuretics. Is this cystitis or pyelonephritis? It is the same for both. Suprapubic pain in cystitis and flank pain in pyelonephritis. aztreonam. You can’t stain a CT. strep and sometime staph. There is itching because of the eggs and feces. frequency. dig. whatever. 1/3 of women with bacteria will develop pyelonephritis. oozing. contact dermatitis. beta blockers. azlocillin. Treatment is lindane or permethrin. * An ultrasound looking for pyelonephritis will show nothing. Might see trails dug under skin in skin creases. like cryo would). ampicillin. diuretics. None will cure the virus anyway. preterm delivery associated with bacterial vaginosis. DO NOT DISTRIBUTE . * Cystitis treated with TMP-SMX or ciprofloxacin for 3 days. Is there an anatomic defect (stone. but you can get glomerulonephritis. So now treatment is ACE-I.

clotrimazole. lotrimin. then look at the slide. Some people may need 4-6 months of therapy. tumor.g. dermatophyton. So you do not know what organism to treat. this way you do not need to do a bone biopsy every few months. only worked 30-40% of the time. KOH melts away the epithelial cells. like athlete’s food. it is the same stuff that makes the lobster/crab shell hard. Ketoconazole also affects the liver due to P450 interaction. athlete’s foot) take weeks for the cultures. nystatin. “Mold in the cold. diabetics are more susceptible to Gram-negatives and anaerobes. bone scan. * Griseofulvin had to be used for 12-18 months for nail infections. even in rheumatoid arthritis. Do not do a bone scan because the red ulceration soft tissue swelling gives too many false positives. You follow the ESR. * Mold treatment with hair/nail involvement cannot be topicals. athlete’s foot spreading. use ESR. Molds (e. immobile. X-rays. calor. It is very anti-androgenic that systemically you are more likely to use it for metastatic prostate cancer. * Fungus is the group. The most accurate test for any infection is culture (few exceptions. then what is the next step? Answer is MRI.Study Notes – Internal Medicine James Lamberg 28Jul2010 * Impetigo can sometimes be treated with topicals like bacitracin or mupirocin. but do the x-ray anyway. then this is just an ulcer. What is the best initial diagnostic test. tender. oral thrush. * X-ray shows osteomyelitis. * If x-ray and MRI negative. vaginal candidiasis. MRI has same sensitivity as bone scan but does not come with the false positives. then treatment. * When do you culture the drainage out of the sinus tract? Answer is never. next step is biopsy to determine organism. microsporon. like herpes encephalitis with PCR). Answer is aspiration. periosteal elevation. Others would be risopus and mucor mycosis in diabetics. If the x-ray shows osteomyelitis. * We don’t use ketoconazole usually. If the SED rate is down then you can stop. if the SED rate is still up then you continue. takes DO NOT DISTRIBUTE . * Do not culture sinus draining tracts due to false positives. not osteomyelitis. good for cryptococcus. You start the patient on 6-weeks of antibiotics after the biopsy. terconazole. yeast/candida in blood. Treatment for 12-weeks. ketoconazole. X-ray very rarely shows anything in septic arthritis. it is very close to orchiectomy at high doses. What is the best initial diagnostic test? CT. Oral thrush. which is why you do the biopsy. fingers for 6weeks. You don’t skip an ECG and jump straight to the stress test. X-ray is always first with osteomyelitis even if you think it will be negative. * When do you get a SED rate? You get it to follow the response to therapy. -------------------------------------------------------------------------------------------------------------------------------------------Osteomyelitis * 57yo male diabetic with peripheral vascular disease and has pain in leg for last 10 days.40 - . MRI. Doesn’t it take 2-3 weeks for the bone to dematerialize enough to see it on an x-ray? Yes. SED rate is useful to determine length of therapy. red. cryptococcus are yeasts. However. Fluconazole is very safe. How do you know what organism to treat? Most common cause of osteomyelitis is staph aureus. Cellulitis with red draining tissue will mess up the bone scan. even if the person has only had the disease for 5 days. culture? Answer is x-ray. -------------------------------------------------------------------------------------------------------------------------------------------Septic Arthritis * 72yo female Catholic nun from Brazil with a fever.” Only mold to worry about in general is skin infections. She has a painful. swollen. Must be systemic therapy. What is the next step? Answer is biopsy. 80-90% cure. * Mold treatment without hair/nail involvement would be any topical. miconazole. Scrape area. some acetic acid. destroyed bone involucrum and sequestrum. dolor. It hurts just below his knee. vaginal candidiasis. It does not work on molds. The only way to know which specific fungus is to do a culture. malassezia furfur. So get the culture then initiate treatment. leaving fungi. Rubor. Articulatory cartilage is amazing stuff. Environment growing in the refrigerator or plants tends to be molds. It is the only one you can treat with topicals because it is superficial. miconazole. Kid comes with toenail infection. then after 6-7 weeks or so you check a SED rate. Inside you at body temperature is yeast. If MRI or bone scan is positive. have a 6-month lag time. heat it up. * The KOH will show the fungi. inside the group are molds and yeasts. It will be contaminated and colonized with skin flora. terbinafine. can also give itraconazole. * Fluconazole is a yeast drug. put some KOH on it. Treatment is based on whether or not there is hair/nail involvement or no hair/nail involvement. * What if the original x-ray were negative. -------------------------------------------------------------------------------------------------------------------------------------------Superficial Fungal Infections * Any form of superficial fungal infections has the best initial test of KOH and culture. Never wait for results of culture to treat. x-ray. econazole. It will not tell you what is in the bone. hot. most common side-effect is gynecomastia. * Molds include epidermophyton. yeast in the beast. effusive knee. Fungi has chitin in the cell wall of the fungus. has an ulcer over the area over past 5 days with a draining sinus tract.

-------------------------------------------------------------------------------------------------------------------------------------------Endocarditis * 27yo man. * Summary: you see fever and murmur. * Say arthrocentesis shows 62. only 40% of disease had treatments. Less than 10% of patients have any of these signs. What is the most accurate diagnostic test for this patient? Answer is culture. arthrocentesis. 700 pages. * Sensitivity of TTE is 50-60% sensitive. So. no prophylaxis needed. biliary surgery. No matter how long you give antibiotics. mitral stenosis. has fever. * What is the next best step in the management of this patient? Blood cultures or echocardiogram? Answer is blood cultures. all these areas. Gram-positives with something like oxacillin. That is why you order blood cultures first. You look in this guy’s eyes and see no Roth spots.g. ANA negative. Gram-negatives with something like third-generation cephalosporin (ceftriaxone). so not used primarily. aortic stenosis. In 19th century. No Janeway lesions. cervix positive in 20-30% of patients. * What about gonococcal septic arthritis? Blood positive in less than 10%. The physicians do tests. Now the most common cause of death from endocarditis is CHF. You won’t get asked diagnosis. bacteria cannot penetrate. * Many physicians will not even take a sexual history because they assume it is unreliable. cystoscopy. increased motilin). Osler lived 50 years before antibiotics were invented. but that is pretty invasive. Treatment is ceftriaxone. Pacemaker. I just lay there. IV drug use. You look in hands and feet and see no Osler nodes. Osler invented residencies in this country and wrote the first comprehensive medical text. but has side-effects (vomiting. most often staph (40%) and could be strep (30%). just cover bacteria present. * Dr. IHSS (HOCM) idiopathic hypertrophic subaortic stenosis. * Non-gonococcal septic arthritis. and murmur. Prophylaxis for endocarditis when something is on the inside. and joint pain.g. pharynx positive in 10-20%. CABG. this is how we think about metastatic disease. if you think there is gonorrhea. get the blood culture. and considering it is 97% water. does not cause bacteremia. give clindamycin. C-section (with valve problem). it DO NOT DISTRIBUTE . There is not specific drug to learn (like ceftriaxone in meningitis). So again. even though it is a foreign body. Now what? MVP. If blood cultures are positive. azithromycin is alright. Erythromycin will cover the mouth flora. quinolones. or pacer in place. culture everything. If TTE is negative. All you need to see is fever and a new murmur. 10% misc. Culture of synovial fluid is over 90% sensitive.000 white cells. whatever. then get transesophageal echo (TEE). So you have some heart problem and are getting a bacterial flinging surgery. What is the sensitivity of a Gram stain? At least 50-70%. the papillary muscle and chordae tendineae will not jump out and reattach themselves. aortic stenosis. no prophylaxis. VSD). Gram positive in less than 25%. CABG. * You’re going to get your teeth cleaned and have MVP. * Treatment is started right away. You look in this guy’s fingers and see no splinter hemorrhages. * Treatment is with two agents to cover Gram-positive and Gram-negatives. coronary arteries are on the outside of the heart. These patients dies of post-infectious endocarditis. uterus is sterile environment. urethra positive in 10-20% of patients. What does that mean? Nothing. * To get endocarditis. hemicolectomy. When do you answer surgery? What is the most important and urgent indication for surgery in endocarditis? Answer is CHF. even after blood cultures. then get transthoracic echo. Are you sexually active? No. do not order scans here. No dose after the procedure. get echo and you’re done. rheumatoid factor negative. When do you wait for results of culture? Never. culture positive in only about 50%. do an aspiration. Blood cultures positive in 25-30%. So for non-gonococcal septic arthritis. mitral stenosis.41 - . no prophylaxis. TEE is more than 90% sensitive. * Prophylaxis for general procedures like dental work is amoxicillin 2grams one hour prior. If TTE is positive. tap the knee. fever. we’re going to find it. needs prophylaxis because it is significant enough to cause sudden death. polys. What type of septic arthritis does this patient have? You have to order tests. no prophylaxis needed. If negative. If patient is penicillin allergic. polyarthralgia (in multiple locations)? Tenosynovitis? That is how you know. 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. -------------------------------------------------------------------------------------------------------------------------------------------Lyme Disease * A bunch of children are brought to the hospital with rash. Only single disease with 100% mortality was endocarditis.Study Notes – Internal Medicine James Lamberg 28Jul2010 huge amount of stress and trauma. Take culture and start to treat. Cardiac catheterization (with valve problem). give prophylaxis if significant regurgitation (murmur). 20% gram negative rods. hemicolectomy. Urine has no red cells. you need a bacteremia causing procedure (e. nafcillin. then you know this is endocarditis. IVU (IV drug use). dental cleaning) and a significant defect (e. do a Gram stain. TTE will miss almost half of endocarditis. SED rate a little elevated (and SED rate is like Rorschach inkblot test. How do we make the diagnosis then? Rectum positive in 1020% of patents. Synovial lining does not have a basement membrane. so bacteria (and antibiotics) pass easily.

use dapsone. 15. * Treatment is doxycycline or amoxicillin. Characteristic about CN VII palsy is that it is bilateral Bell palsy. There is no chlamydia trachomatis vaccine. * The fascination from Lyme comes from parents coming back and back and back until the disease was described. Viral load tells the future. No need for tick analysis. * When to start HIV medications.000 cases per year and practically no one dies. The rate of decay of T-cells is dependent on the viral load. Reverse transcriptase inhibitors are -vudine drugs. -------------------------------------------------------------------------------------------------------------------------------------------Human Immunodeficiency Virus (HIV) * Asymptomatic patient with HIV presents to your office asking what medications they should be taking. saquinavir. You can get joint problems. at risk for pneumocystis pneumonia (PCP). Third line is atovaquone. meaning T-cells from > 500 down to < 200? Answer is viral load. how aggressive the diseases is. MAC). patients were taking pills all the time but still dying anyway. Lyme in Connecticut (near Yale. stavudine (D4T). * Zidovudine (AZT) causes anemia. What determines what length of time you develop AIDS. Without clinical manifestations. Mortality on Lyme is negligible. for minor stuff like rash or Bell palsy or joint problem.g. You can get just the rash. or just any of them. remove the tick. If you have a positive serologic test and no symptoms.42 - . Lyme. CMV with oral ganciclovir also not used. DO NOT DISTRIBUTE . Serology for IgM and IgG is lousy because it cannot distinguish well between old and current infection. * Tick ixodes scapularis has to be attached for 24-72 hours. reverse transcriptase inhibitors. but can get nasty arthralgia later on. Aerosol pentamidine is 4th line and practically an extinct drug. HIV drugs. You don’t feel 400 or even 350. If cardiac or neurologic problems. Didanosine (DDI). * Diagnosis is clinical manifestation. based on T-cell count of viral load? CD4 under 350 or viral load over 55000. * No mortality benefit with antifungal prophylaxis with fluconazole. * There is no malaria vaccine. serology is useless for Lyme. Prophylaxis is based on what you are at risk of today. 3rd highest income per capita in world). cardiac problems. It’s like a train heading toward a cliff. Physicians send kids home and say children have juvenile rheumatoid arthritis. possibly a few AV block cases. this is not like syphilis with VDRL and RPR (diagnosed with syphilis even if no symptoms). Is prophylaxis based on the T-cell count or the viral load? Answer is T-cell count only. T-cells tell the present. at risk for mycobacterium avium intracellular (MAI. It has a high incidence with the wealthy population. Positive blood test with no symptoms means no Lyme. If you get a rash. prophylaxis with TMP-SMX. prophylaxis with azithromycin. But. No need to treat. ritonavir. This is how Lyme disease was described. Lamivudine (3TC) has such few side-effects that the placebo has more side-effects during testing. No need for serology (positive serology wouldn’t matter). These are very effective. * Asymptomatic HIV-positive man comes to your office with 12 lonely T-cells. 15000 cases per year and it is very hard to die from. protease inhibitors. Worry when you get near 200. This means you cannot die from the virus. * 26yo woman who gets bitten by a tick on her buttocks. With these 5 medications. All the children in an area won’t get JRA at the same time. * 200 T-cell or less. 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. nelfinavir. and some neurologic problems (e. and that is the problem with diagnosis today. zalcitabine (DDC). Rifabutin is a dead drug. or just the neuro. * 50 T-cell or less. 95-98% of patients who are HIV positive without treatment will die from AIDS. Then what? Do nothing. there is a Lyme vaccine. Side-effects of DDI and D4T are neuropathy and pancreatitis. not by screening thousands of compounds. You do not treat asymptomatic serology. Indinavir. They kill a virus so we call them -avir. Patient may get a rash sometimes. use ceftriaxone. Moms look into their pediatrics textbook of medicine and decide to stop back to the doctor’s office the next day. you do not have Lyme. 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. She has no symptoms. * Less than 200 T-cells and less than 50 T-cells is what you need to know. * About 5% of patients who are HIV positive will never develop AIDS. how fast will T-cells drop. Normal is around 600-1000 T-cells. * Protease inhibitors were created de-novo. 3-30 million people go blind annually because they don’t have a dollars worth of doxycycline or erythromycin.Study Notes – Internal Medicine James Lamberg 28Jul2010 doesn’t mean anything). What do you do for this patient? Answer is tickectomy. Bell’s palsy). * Use 2 nucleosides and a protease inhibitor (PI) and viral load goes to undetectable in 80-90% of patients. and when to start anti-retrovirals. Second highest incidence of Lyme in Westchester NY which has the 2nd highest per capita income in the world.

* When the antibodies attach to the antigens. what. stop medications. If you do see intact blisters. This woman has a 50% six month mortality. -------------------------------------------------------------------------------------------------------------------------------------------Post-Exposure Prophylaxis * 26yo surgical intern is stuck with an HIV positive needle (needlestick) in the O. who tells him afterwards. Mother to child transmission is about 1:20 with meds and about 1:3 or 1:4 without medications. they’re on it for 3-months. So how much has the death rate from HIV dropped in the United States? Answer is 80-90%. average life expectancy for a woman is 79 years. Half of those children will be infected and most of those children will be dead by age 5. DO NOT DISTRIBUTE . What is the next best step in management. event. Her T-cell count is 35. Do not let her die because she is pregnant. they are undetectable. they are very fragile and easily breakable. MD -------------------------------------------------------------------------------------------------------------------------------------------This section is very picture-intensive. -------------------------------------------------------------------------------------------------------------------------------------------Kaplan Videos (2001) – Dermatology with Dr. You took a transmission risk of 50% and brought it down to 2-3%. Answer is duration of contact with infected semen for 4-5 hours.43 - . In Africa. The blisters are so superficial that by the time the patient presents to the physician you rarely see intact blisters. In South Africa. less than 400 children born HIV positive. Oral transmission rates are not really known.S. You took a fatal prognosis with HIV. death rate is higher since there is no milk formula available. mainly due to the fact that 1/3 of women in prenatal clinics are infected with HIV. With 2+1 therapy. patient is on medications forever.000. and made it 80-90% not fatal. Have gratitude in your attitude for access to the medical therapy we have. * Put patient on 2+1 therapy. and it breaks apart and blisters up. it is a difficult thing to study. -------------------------------------------------------------------------------------------------------------------------------------------Bullous (Blistering) Diseases * Pemphigus vegetans is a rare variant of pemphigus vulgaris. Over 10 years. * 33yo man has unprotected sex with an HIV positive girl. * Pemphigus vulgaris is a blistering disease. how long do you continue the medications? If you keep patient on medications for 5 years. by her attending physician. You’d rather be alive with a high LDL and HbA1c then dead with normal levels. 16 HIV medications were approved and new ones coming out all the time. but most of the skin will be denuded. Which drug caused this? Answer is indinavir. so quickly review an image for each disease discussed.000.Study Notes – Internal Medicine James Lamberg 28Jul2010 * So protease inhibitors help drop viral load to undetectable in 80-90%. viral load of 600. You start HIV medication for < 350 T-cell or viral load > 55. * Once you start HIV medications and you go undetectable. Pemphigus vulgaris is an autoimmune disease of the skin. the virus can come back the next day. Anal receptive is about 1:100 (1%) per shot. What is the next best step in the morning? Answer is give 2+1 for one month. * Protease inhibitors have side-effects of hyperglycemia and hyperlipidemia. Needlestick exposure is about 1:300 episodes/contact. less than 4-5 hours. the skin can no longer stay intact. * Which HIV medications (nucleosides or PI) are teratogenic? None of them. * In the United States. These antibodies are found in the intercellular spaces between epidermal cells. 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. and that is a great good. Patients with pemphigus vulgaris have auto-antibodies that respond to antigens that are found in the epidermis (top layer) of the skin. comes back with terrible flank pain and hematuria. 10 seconds? The time duration of the coitus. it is 32 years. * Pediatric HIV is virtually non-existent in the U. transmission rate drops even further to about 2%. load. * Over 70 years. Answer is give 2 nucleosides and 1 protease inhibitor for one month. Answer is not surface area differences. So. * AZT alone in pregnancy results in about an 8% transmission of HIV. What do you do for this patient? Answer is 2+1 now. C-section not routinely indicated. Man is only exposed for about. only if viral load is not under control. there are about 5 drugs created for tuberculosis.R. Risk is about 1:1000 for male to female (vaginal). -------------------------------------------------------------------------------------------------------------------------------------------HIV Transmission Risk * 32yo woman who is pregnant and is HIV positive. She is at 7 weeks of pregnancy. * Why is male to female transmission higher than female to male? Answer is not vaginal trauma.. Marsha Gordon. * 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. causes stones. Risk of transmission through breast milk is equal to unprotected sex or equal to the risk from the delivery itself. * Risk of transmission is about 1:3000 for female to male (vaginal).

It is believed that this is the time needed to recruit and sensitize the lymphocytes. It is mast-cell induced. develops a photosensitivity. and fungicide hexachlorobenzene may be a precipitant. * Pemphigus and pemphigoid tend to heal well with treatment. DO NOT DISTRIBUTE . * There will be intact. Pemphigus presents classically around ages 30-40. Immunofluorescent will show lighting-up. so scarred tongue. If the urticarial hive lasts less than 24 hours then it is urticaria. steroids. Erosions in the oral mucosa may occur before skin is involved. Iron may be a precipitant. * You see vasodilatation. blisters with some denuded/eroded areas.Study Notes – Internal Medicine James Lamberg 28Jul2010 * This disease affects the skin and the oral mucosa. * Precipitating factors for PCT is alcohol. the blisters are deeper. they develop hypertrichosis. It may be slightly raised. lymphocyte mediated. scars around mouth. This condition does not heal well. This does not generally involve the oral mucosa. -------------------------------------------------------------------------------------------------------------------------------------------Porphyria Cutanea Tarda * All porphyrias relate to abnormalities of heme metabolism. Second. causing hive swelling. tense. they look like they are getting a tan. * The second exposure will result in a reaction within 3-4 days because they have been sensitized. * If a patient is given an antibiotic and are doomed to develop a morbilliform rash. it heals with scaring and heals slowly. We also treat with blood-letting (phlebotomy) to try to drain off excess iron. causing hive pinkness. think pemphigus but realize the actual diagnosis is made by biopsy. including lots of histamine and mediators. new hives will continue to present over weeks as long as the antigens are present in the system. at the DE junction. it attaches to IgE antibody on the mast cell and causes release of the mast cell package. the first time they are exposed they will not develop a rash from somewhere between 10days to 2weeks. * Any individual hive will last up to 24 hours. they react at the DEJZ. a linear line. * Many disease present looking similar to pemphigus vulgaris. * Biopsy must show the epidermis breaking apart one cell from the other. now we treat with high dose prednisone and steroidsparing medications like azathioprine. * Morbilliform drug rash often seen with antibiotics. If you see a slide with blisters and denuded areas. -------------------------------------------------------------------------------------------------------------------------------------------Hypersensitivity Reactions * Urticaria is the classic type I hypersensitivity eruption.44 - . * Bullous pemphigoid is an autoimmune disease of the skin with antibodies reacting against antigens at the dermoepidermal junction zone (DEJZ). First. so women who are on birth control pills or hormone replacement. * Porphyria cutanea tarda (PCT) is the classic dermatological porphyria. The blisters are tougher. and when proper allergen comes along. You see leakiness of the vessels. The top of the scalp is another location. They almost never present with intact blisters. * Two other skin manifestations besides blisters. * Clinically we see blisters and erosions. The disease was fatal prior to discovering corticosteroids. ages around 70-80. As a result. * Cicatricial pemphigoid is a less important variant and does scar even with treatment. This is believed to be a type IV hypersensitivity eruption. so middle-aged alcoholic with blisters. * Bullous pemphigoid presents in an older population. tend to be tense. Estrogens are a classic precipitant. and often are intact when they present. blindness from eye involvement. Mast-cells have IgE antibodies affixed to them. The classic place the hair is seen is at the tops of the cheeks. It almost exclusively involves the mouth and eyes. However. patients develop hyperpigmentation. * Pemphigus foliaceus and pemphigus erythematosus are more superficial forms of pemphigus. you will get an urticarial reaction probably within 30 minutes to an hour at the most. * Treatment is to remove precipitating factor and use anti-malarial medication chloroquine. they become hairier. They do not react with anything in the epidermis per say. The metabolites that accumulate are photosensitizing. meaning if the patient is allergic to penicillin and you give them penicillin. and also immunofluorescence can show the antibodies being deposited in little circles around the epidermal cells. * Bullous pemphigoid biopsy will show blister with entire epidermis lifting and separating from the dermis. Bullous pemphigoid is seen in a geriatric population classically. This is important because other diseases can look like hives. * The face also can be involved. * Morbilliform eruption is a faint pink morbilliform (measles-like) eruption. a differentiating feature between the two. classically the dorsum of the hands. Skin that is exposed to the sun. * These are immediate reactions. It is a slow improvement and may take up to a year.

The blisters have purulent material in them and are teeming with staph. Tinea capitus can scar if not treated. It is benign. * Erythema multiforme refers to target-like lesions. watch fluid and electrolytes. the same reaction occurs. extending over time. scaly border. Because the patient is debilitated. Whatever the formation. * Tinea capitus usually seen in kids with a patch of hair loss (alopecia) or thinning. poor kidneys or poor liver. we do a biopsy and send it for frozen section because we want an answer quickly. If you can’t tell the difference. Because eye involvement can occur. The blisters are intact and if you open and do a KOH prep you will see it teeming with dermatophytes. The infection can get down into the roots so topicals will not reach. * Fungal infection of the toenails is onychomycosis. Classic pattern is annular (round). The entire thickness of the epidermis is lifted and separated from the dermis and is necrotic/dead. usually involving the soles of the foot. * The multiforme means it can take many forms. * Certain strains of staph exude a toxin. So you see fluid and electrolyte abnormalities. we see complete necrosis of the entire epidermis. This is almost always caused by a drug. Think about this if called to a neuro management unit for a major skin disorder. but don’t forget it could be a tinea corporis. In one are. Mortality 25-50% even with appropriate treatment. * TEN prone to electrolyte abnormalities and infection. carbamazepine. If you give the drug back. Specifically with herpes. Tinea cruris is fungal infection of the groin. Within a short period of time. * Staphylococcal scalded skin syndrome is from staph that exudes exfoliatin toxin. Sometimes the skin is scaly and peeling. Many times you will think this is just an eczema. * If any mucus membrane involvement. giving a permanent scaring alopecia. Tinea pedis classically involves the interdigital webs between the toes. In SSS. older or very young. phenytoin. elevated white count. Classic example is a bull-shot with a dusky bluish color in the center and a red rim around. * Honey colored crust. think impetigo. which is a major cause of death in TEN. May have fever. With skin involved. must have an ophthalmologist involved in this care.Study Notes – Internal Medicine James Lamberg 28Jul2010 * Spectrum of hypersensitivity reactions begin with erythema multiforme. * There can be 100% sloughing of skin. * Stevens-Johnson refers to more than minor mucus membrane involvement. Classically you see hemorrhagic crusts of the lips and oral mucosa. but the main site is distant from the skin (e. red. the skin begins to bubble-up and literally sloughs off. So there may be a blister in the center with a red rim around. classically seen on the palms. We do not know why this happens. These patients will likely have skin involvement as well. There is a blistering form of tinea pedis. patient is prone to infection. * On frozen section. cortisone (prednisone). patient may not be eating well. targetoid appearance.g. they cannot break down this toxin and it spread throughout the body. penicillins. Say in addition the patient is pretty sick. thus will go away if you remove the offending agent/disease. This toxin can cause the skin to blister. Say patient has impetigo that is caused by one of these types of staph (bullous impetigo). With mucosal involvement. sulfonamides. These patients are tremendously ill. * To make a TEN diagnosis. * TEN treatment is stop medications. steroids are highly controversial because they mask infection. DO NOT DISTRIBUTE . they develop either a blister or a red mark. while TEN can be caused by antibiotics. -------------------------------------------------------------------------------------------------------------------------------------------Bacterial Skin Infections * Tinea pedis (fungal infection of foot) caused by dermatophytes (fungus that attacks the skin). abdominal abscess). in the exact same location. pus bumps. you will see the honey-colored crust and blisters around. it will be target-like. it heals. the involvement has to be very minor to be called erythema multiforme. If you take away the drug.45 - . * Fixed drug eruption generally heals with a dark mark that can take a long time to fade. but is treated very differently. put in laminar flow room to prevent infection. * TEN can look very much like staphylococcal scalded skin (SSS) syndrome. Classically involves the palms and soles. However. * Toxic epidermal necrolysis involves skin that is confluently red that burns or feel tender. patient can get recurrent erythema multiforme with each outbreak. the break is way high up in the epidermis. Sometimes there will be a few little pustules. and finally to toxic epidermal necrolysis (TEN). Treatment of SSS with antibiotics. exfoliatin. * Erythema multiforme often seen to drugs and also infection (herpes and mycoplasma pneumonia). do a culture (takes weeks) or a KOH prep. * Treatment of tinea capitus is oral anti-fungals. Caused by staph or group A strep (pyogenes). a recurrent infection. * Treatments involve covering for staph and for strep. then to Stevens-Johnson. * Stevens-Johnson has a mortality of 5-10% even with appropriate treatment. barbiturates. * Disease can last 2-3 weeks. so like a 100% burn. * Erythema multiforme is self-limiting. * Tinea corporis can be very subtle with a tiny pink scaly area. bullous tinea pedis. they can be seen on other parts of the body. elevated liver function tests. allopurinol. * Fixed drug eruption refers to a situation when a patient is exposed to a drug they are allergic to. it is just a curiosity.

tender plaque. * Furrows or linear burrows may be a clue. * Think about any other bacteremia here also. Senile purpura is seen in elderly patients with fragile blood vessels and connective tissue. CN VIII. the blisters begin to develop. * Meningococcemia present with a brief upper respiratory infection. -------------------------------------------------------------------------------------------------------------------------------------------Viral Skin Infections * Herpes is a viral infection that classically involves the mouth or genitalia. * HIV-positive patients can quickly develop tertiary syphilis with CNS changes. decreased glucose. So if you see the patient and think it is a chancre. Can be caused by a mixed infection or a strep infection. tinnitus.Study Notes – Internal Medicine James Lamberg 28Jul2010 * Exfoliatin toxin causes skin to exfoliate. * Secondary syphilis appears 6-8 weeks after chancre. Oral herpes can be brought out by sun as well. * Treat necrotizing fasciitis with antibiotics and it absolutely requires surgical debridement. Only an average of 11 mites on entire body. -------------------------------------------------------------------------------------------------------------------------------------------Other Skin Infections * Scabies is caused by human mite. Petechia are non-blanching purple areas of the skin. or kidney stone. Strep can travel extremely fast. Next stage is a fever and mental status changes. such as cold sores. * Herpes zoster is disseminated if more than 20 blisters outside of a dermatome. where they can spread across the planes and cause damage very quickly. This is shingles from herpes zoster. and the interdigital webs of the hands. Usually pretty evident. sarcoptes scabeii. Not much to say about warts. * Here you do a frozen section to differentiate from TEN. * Herpes comes and goes. the blood test should be positive. axilla often involved. Patient may present to physician thinking they’re having a heart attack. It causes an extremely itchy bumpy area. you need to do a dark field exam of the chancre looking for spirochetes. many types. The lesions have a smudges look and given time they will become vesicular and necrotic with a slate-gray center. such as penis and scrotum. A day later. If can be so acute and fulminant that there isn’t enough time. or sciatica. warm. * If you see a zoster involving the ear. * Do Gram-stain of CSF looking for organisms. can be from 10-90 days. Lips can be very swollen. increased protein. * Treatment for SSS syndrome is anti-staph antibiotics. Average time of onset of chancre is 3-weeks after exposure. Often we cannot do a culture so treat for what you think it is (staph or strep). extending down a dermatome. Itchiness due to stool. DO NOT DISTRIBUTE . Presents with red. especially areola. If you culture or Gram-stain skin. facial palsy. If TEN. think about Ramsey Hunt. nontender classically. treponema pallidum. But we must treat quickly. vertigo. you see intact epidermis expect for very superficial blistering. associated with nontender adenopathy. Other places classically involved are breast. think meningococcemia. If you see fever and rash. * Clinically you see groups of blisters on a red base. you won’t see anything because the staph is at a distant site and you’re getting the result of the toxin. * Patients need a good general workup for any herpes zoster a month after healing because they may be immunosuppressed for a variety of reasons. see oval salmon-colored patches over the body with palms and soles involved. It may be difficult to distinguish at the bedside from TEN because you see the skin sloughing off. At this point. The first case of a cold sore for a patient can be extremely angry if they have no immunity to it. we can do a biopsy and see strep very deep. You need to scrap a spot and look for eggs. 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. The average time when the blood test turns positive is 4-weeks. This patient is not controlling their zoster infection Admit patient to hospital and treat aggressively. They can get large purpuric areas with very minor trauma. Mark with pen to determine if treatment is working or if cellulitis extending. Not everything that is purpuric is not a major infection. mostly because those are the common areas of inoculation. * Necrotizing fasciitis (flesh eating disease) is a medical emergency. It can be seen in other areas including the eye.46 - . * Syphilis starts with a chancre (primary). then take them off antibiotics. Here in SSS syndrome. This means there is hematogenous spread. * You may not see signs of meningeal irritation. * If there is a question. from ankle to thigh in a single day. a reactivation of latent varicella zoster virus (chickenpox). * Warts caused by human papilloma virus. Some believe you need an LP. * Say you see many groups of blisters on a red base. Generally it starts with a cellulitis and quickly the organisms go deep and make it to fascial planes. * Cellulitis usually caused by staph or beta-hemolytic strep. * If trigeminal ophthalmic division is involved with herpes you need an ophthalmologist. like staph bacteremia. Superficial at the granular layer of the skin. Generally zoster begins with pain. associated with lymphoproliferative diseases. hard. often arising in times of stress.

Ask about family atopy. and III (mets). This is benign. irregular color. sheering forces (slipping down in bed). sometimes the scalp. Stage I is non-blanching redness. * Kaposi sarcoma seen in immunosuppressed population (AIDS. If it presents at this stage without dermis involvement there is 100% cure with proper excision. Melanomas are asymmetrical and irregular.Study Notes – Internal Medicine James Lamberg 28Jul2010 -------------------------------------------------------------------------------------------------------------------------------------------Pigmented Lesions * Pigmented lesions come in all shapes and sizes. Patients will have asthma. It classically begins with a herald patch. hay fever. friction. benign. Bluish plaque like discoloration. you see well demarcated rash only at location of problem (e. So they react in an expected way to the staph that is on our skin. in the area around the nail. * Most common melanoma is superficial spreading type. Locations are the nasal labial folds. the growth is out of control. * 75% of squamous cell carcinomas on the skin are sun-induced. * Eczema (dermatitis) can be asteatotic. around 1%. * Nevus with irregular border. Protein surrounds the vessels causing fibrin cuffs and preventing oxygen exchange so tissue becomes hypoxic and breaks down. feet) with high mortality and lentigo malignant type seen on the sun exposed areas of elderly people and has good prognosis. broken blood vessel on it possibly. we can cure the patient in most cases. scalp. Stage IV means all the way through to bone or muscle. but it is still irregular. but the majority of patients do not develop cancer. * Treat by removing things that cause allergy. color. where it is only present at the epidermis. and eczema. moisture from incontinence (urinary or fecal). rubbing. * Seborrheic eczema is a chronic condition with redness and scaling in classic locations. Lymphocytes are destroying nevus. usually staph. poison ivy in linear blisters). rarely the palms. Generally do not metastasize. Decubitus ulcers caused by pressure. * Stasis dermatitis begins with venous insufficiency. Skin can be thickened from scratching. * Compound nevus. benign. symmetric. overgrowth of top layer of skin. Some of the nevocytes are at DE junction and some down into dermis. 15% of melanomas. 70%. most common of all cancers. Once a malignant pigmented lesion has occurred. This has an in situ phase lasing 6months to a year. Other types are acral melanoma (hand. Should be removed. In allergic contact dermatitis. Sometimes you see a pus bump. eyebrows. -------------------------------------------------------------------------------------------------------------------------------------------Nail & Hair Disorders * Acute paronychia is an infection. with red itchy patches in the flexures.47 - . meaning eczema simply on the basis of dryness. chemotherapy) and elderly (Mediterranean). Benign pigmented lesions tend to be symmetric. It never involves the palms. Can cause nail changes (pits) and generally nail dystrophy (onycholysis). They have lots of IgE in system. oval slightly scaly salmon-colored patches over the body. symmetrical. The exception is squamous cell carcinoma of the mucosa (lip) where there is a metastatic rate 10-20%. Formed elements in blood cells like hemosiderin leave the dark spots. lymphoproliferative. * Pityriasis rosea looks like secondary syphilis. If we can find them and treat quickly. Generally culture but always cover for DO NOT DISTRIBUTE . is a benign lesion with the melanocytes found at junction (epidermis/dermis). diameter smaller than pencil eraser. Melanomas start with melanoma in situ. Seen often in patients who get manicures. * Contact dermatitis from irritation or from allergic contact dermatitis. not well understood. * Greasy stuck-on appearance are seborrheic keratoses. probably a neoplasm of epithelial cells likely lymphatic and small blood vessels. * A junction lesion. They have a low metastatic rate. benign. Is this lesion symmetrical? Yea. this is melanoma. Skin gets so dry that is simply breaks down. It appears and immediately invades. * Actinic keratoses refers to an area of the skin which is scaly and caused by sun (sun exposed area). Can turn into squamous cell carcinomas.g. around ears. Get a VDRL to rule-out syphilis also. symmetric. Stage II is very superficial breakdown. * Decubitus ulcers are defined in stages. border. Keep in mind symmetry. Prognosis is based on level of depth of invasion. * Stages are I (skin). Diagnosis with biopsy. * Dermal (intradermal) nevus is skin colored. II (lymph). Next most common is nodular. They are precancerous. -------------------------------------------------------------------------------------------------------------------------------------------Papulosquamous (Scaly) Eruptions * Psoriasis is silvery scale on a red base. Stage III is full-thickness skin breakdown but not to fascia. sometimes just red and tender. Sarcoma is a misnomer. * Halo nevus is a symmetrical halo of lightness around a nevus. * Atopic (allergic) eczema is usually seen in atopic families. Usually involves the knees and elbows. * Basal cell carcinoma has pearly raised border with crust. specifically to staph. look at ABCD. * Nodular melanoma may be more symmetrical than others. but symmetry matters.

if from dermis it is epidermoid and if hair follicle then pilar cyst. The most common types of cancers of the gastrointestinal tract are adenocarcinomas. * Clubbing can be seen in cyanotic heart disease as well. like scleroderma. surgery. They involute each year such that by the time the child is 9. * Traction alopecia comes from chronic pulling of the hair so much so that the roots are destroyed. * 90% of cysts on scalp are pilar cysts but you really can’t tell until you remove them. There will be periosteal thickening of the distal phalanx and often gynecomastia. Capillary hemangiomas also called strawberry hemangiomas. The lower part near the GE junction is columnar epithelium. * Telogen effluvium seen after patient goes through tremendous physiologic stress. The body is stressed so it is shutting off non-essential functions like hair growth. Alopecia areata totalis covers all the hair in the head. So decompress. * Digital mucus cyst are soft. affect the esophagus greatly. so anal cancer would be squamous cell carcinoma. The UES and LES will be at high resting pressure then DO NOT DISTRIBUTE . Either way. all you see is a nodule. * Androgenetic alopecia is male-pattern or female-pattern baldness. They are benign. * Hypertrophic osteoarthropathy looks like clubbing except there is tenderness at the distal fingers. If there is no punctum connecting it to the surface. Tophi is sodium urate crystals deposited in the skin. sometimes many of the hairs will all go into a resting phase (telogen). Also benign. * Alopecia areata is oval or round patches of complete hair loss. By the end of the first year they generally stop enlarging and involute. * Esophagus is made of smooth muscle except for the very top where there is some skeletal muscle. universalis covers all the hair of the body. * Most of the esophagus is squamous epithelium. It depends on where the cyst originates from. 90% have completely disappeared. Seen more frequently in obese patients possibly more frequently in diabetics. Treat quickly because if swelling is great enough you can impair the blood supply to the distal tip of the finger. It is due to deeper dermal vessels. That skin keeps making oil/sebum but is in a pocket. could be a collection of mucopolysaccharides (benign and we drain) or a herniation of a joint sac. capillary and cavernous.48 - . It can also involve the nails. There are two types. so don’t do it. treat with antibiotics. what is the diagnosis or how do you make the diagnosis? * Hypopharynx empties food into the upper esophagus via the upper esophageal sphincter (UES). Associated with lung carcinoma. MD -------------------------------------------------------------------------------------------------------------------------------------------Gastroesophageal Reflux Disease (GERD) * Esophagus is a simple structure. The history makes the diagnosis here. This is completely benign. no need to worry. That is why staying sitting up after eating is a lifestyle modification for GERD. * Disease of smooth muscle. Seen in patients who wear tight braids or tight pulling. it grows with the patients. * Acrochordons (skin tags) are benign and not associated with internal malignancy or anything else. soak. It is believed to be an autoimmune type of disease but poorly understood. Often begins in 20s-30s and continues throughout life. Uric acid begins to deposit in the joint. It is sometimes seen in a familial setting but most often in a patient with chronic lung problems. Over time it will deposit in skin giving chalky subcutaneous masses called tophi. This is a permanent scaring alopecia. These hairs will grow back. * Cavernous hemangioma appears in infancy and persists. There is squamous epithelium at the anus again. * Sebaceous cysts divided into epidermoid cyst and pilar (trichilemmal) cyst. Disease such as muscular dystrophies that affect skeletal muscle could cause disturbances in the upper esophagus. Asher Kornbluth. with nail dystrophy. delivery of a baby. the new hair pushes out the old hairs and there can be an enormous amount of hair loss. drain. infection. * Hemangiomas are benign collections of blood vessels. When new hairs begin to grow in a month or two. So all the areas of the esophagus are at low pressure at rest then higher pressure when moving food.Study Notes – Internal Medicine James Lamberg 28Jul2010 staph. Either way. * Does food travel down the esophagus by gravity? No. such as emphysema. where the lower esophageal sphincter (LES) exists. generally appear early in life and enlarge during first year of life. but gravity does play a role. -------------------------------------------------------------------------------------------------------------------------------------------Benign Skin Growths * Gout is caused by chronic elevated uric acid levels. but there will be a few months of hair loss. -------------------------------------------------------------------------------------------------------------------------------------------Kaplan Videos (2001) – Gastroenterology with Dr. Could be a personal or familial tendency. Food travels down to the stomach at the gastroesophageal junction. bronchiectasis. Given symptoms. * Food travels down the esophagus by ordered (sequential) peristalsis. causing joint pain. skin epithelium or hair follicle epithelium invaginates under the skin and makes a pocket. Biopsy of this is difficult and causes lots of bleeding. tuberculosis. * Clubbing refers to a distal bulbous enlargement of the finger tip.

then refluxing into the lungs and causing a chemical irritation of the bronchi. but solid foods are difficult (mechanical dysphagia). can lead to Barrett esophagus. pantoprazole. When food hits the upper esophagus you get secondary peristalsis. However. * Say patient has chest pain. also known as inappropriate relaxation of the LES at rest. not necessarily correlating to how bad the symptoms are. Barrett patients should undergo surveillance endoscopy at some interval (e.49 - . * GERD medication for mild symptoms with longer relief is the H2-receptor antagonists. * Chronic acid exposure at the lower esophagus. this is a key symptom if associated with any disease. chocolate. Antacids do not eliminate the acid. * Barrett esophagus does not hurt and you can’t see it on an x-ray or barium swallow. Once confirmed. * Nocturnal means it awakes the patient at night.” * 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. subxiphoid. * Barrett esophagus can lead to adenocarcinoma. or fatty foods because they opens the LES. That is very suggestive that the symptoms are from GERD. hoarseness. So even if you LES is wide open and you reflux all day. Avoid foods like caffeine. “A chance to cut is a chance to cure. then you should start treating the patient. That does not mean all patients should get this. asthma. esophagitis). loss of peristalsis near the junction. What do you think is the most likely diagnosis? GERD. You may even find adenocarcinoma once the entire esophagus is removed. radiating up. pain with speaking.g. allergy). but redness is non-specific (e. You see these pressure spikes and dips on esophageal manometry. Nearly all of these are available over the counter because they are generally safe DO NOT DISTRIBUTE . Makes you Go. * 32yo man comes to the ED for substernal chest pain of two hours duration. * Symptoms of GERD outside the esophagus include laryngitis. Theoretically the patient will stop making all their acid and become achlorhydric. They can swallow liquids and soft foods. the reflux is neutral (non-acidic) so causes no major damage. * Mnemonic: MG. He says that he sometimes gets the pain while lying in bed at night. * GERD treatment begins with non-invasive lifestyle modification. which is why we are about this finding. * Low grade dysplasia management is treat GERD aggressively for a few months then re-biopsy. * GERD treatment after lifestyle is medication. famotidine. Patient has longstanding GERD and presents with dysphagia.g. * Diagnosis of GERD is made by history. ranitidine. 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. * Your only chance at cure for any GI tract cancer is resection. Most patients with GERD do not get Barrett esophagus and most patients with Barrett esophagus do not get adenocarcinoma. nizatidine. The pain was probably burning. chronic nonproductive cough. lansoprazole. The magnesium is not absorbed and causes osmotic diarrhea. These drugs inhibit the parietal cell from secreting acid. cardiac is ruled out. So acid-induced bronchospasm. * GERD medication for mild symptoms would be antacids if sporadic like magnesium hydroxide or calcium carbonate. * 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. do esophageal resection because it is very likely to develop cancer. rabeprazole. they buffer it. His physical exam is unremarkable. 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. He is given sublingual nitroglycerin and notes his chest pain worsens. Barrett esophagus is metaplasia from squamous to columnar mucosa at the distal esophagus. Other causes include decreased saliva in smokers as saliva buffers acid. Avoid cigarettes smoking because it dilates the LES and decreases esophageal mucus. * Primary peristalsis begins when you swallow something. Aluminum gives you minimum stool (constipation). barium swallow. The endoscopist can suspect Barrett because the color of Barrett mucosa is more red than the surrounding mucosa.Study Notes – Internal Medicine James Lamberg 28Jul2010 going to low pressure to allow food to pass. GERD. * 24h pH monitoring is the gold standard for diagnosing GERD. or x-ray because those do not show you that acid is coming back up in waves. Single best drugs are proton pump inhibitors (PPI) like omeprazole. * Peptic stricture is a smooth tapering of the lower esophagus due to chronic GERD. You can only diagnose it with endoscopy with biopsy. You do 24h pH monitor and it shows distal to mid esophagus pH is 2-3 during the 24 hour period. esomeprazole. Tell patient not to lay down within an hour or so of eating. * Gastroesophageal reflux disease (GERD) is most commonly caused by LES laxity. He is otherwise free of symptoms except a non-productive cough the he has had for the past month or so. * Gold standard is not endoscopy. Side effect of magnesium hydroxide antacids is diarrhea. 1-2 years depending on dysplasia grade). Examples are cimetidine. decreased smooth muscle function due to scleroderma. Patient wears a pack like a Holter monitor for that time. * Most common causes of chronic cough are: post-nasal drip (e.g. Remember that common things happen commonly. Primary peristalsis is voluntary and secondary peristalsis is involuntary. alcohol. Histologically it looks like small intestine cells. Over time they will have trouble with soft foods then liquids.

* 32yo woman with motility dysphagia. but there is also no motility to wash the acid back down so the reflux can be very severe. which is a bad price to paid for heartburn. the esophageal smooth muscle is replaced with collagen and LES replaced with collagen. This is classic for scleroderma. the final pathway to acid secretion is via the hydrogen-potassium ATPase pump. The beak is the contracted LES. there is invasion of the neural plexus that causes contraction. The symptoms have not worsened at all over this period and the physical examination is unremarkable. More so. Or another example say the patient is symptomatic and no longer wants to take medications. Odynophagia means pain with swallowing. The next step is surgery. So inhibition will result in contraction. * If there is progressive narrowing then suspect mechanical dysphagia. the patient will have dysphagia. H2-blocking reduces but does not eliminate acid because parietal cells are stimulated by other things.e. such as tardive dyskinesia. a Nissen fundoplication. * There is no good treatment here other than treating reflux as aggressively as possible. Esophageal manometry shows flat-line of no peristalsis but the LES is also flat-line (low pressure).g. then went to H2-blockers. sclerodactyly (thick tight skin). Motility dysphagia has symptoms that do not depend on the size of the food. It tightens the LES by simulating cholinergic receptors. then PPIs. He continues to have the pain. There are some others that cause chest pain because the esophagus goes into tight spasm. * Histamine binds to parietal cells and stimulates the release of acid. You do a 24h pH monitor and the pH is still 2 or 3. Cisapride was very effective. Why don’t we use metoclopramide as primary treatment? Because dopamine receptors are also found in the brain. telangiectases. go straight to the PPI medications. What is the next step in the evaluation of this patient? * Dysphagia means difficulty swallowing. * Limited systemic sclerosis is also known as CREST syndrome: calcinosis. PPIs are also available over the counter more recently. esophageal dysmotility. * Metoclopramide inhibits dopamine. it increases gastric motility and emptying so acid is put further downstream. Whatever stimulates the parietal cell. * You need esophageal manometry to diagnose the particular kind of motility problem. think of an x-ray (e. * With achalasia. the surgeon cuts the muscle fibers of the LES so it is permanently opened. She has occasional difficulty swallowing liquids. * Nissen fundoplication is usually done laparoscopically. and inhibits CYP450 so be careful with drugs like warfarin and theophylline. The LES is open so they get reflux. * If you do endoscopy and see erosive esophagitis. increasing the chance of polymorphic ventricular tachycardia. Say you do a manometry and see flat-line with no spikes and the LES does not relax. * Cimetidine can cause gynecomastia in men. Raynaud phenomenon. you see a bird’s beak esophagus with barium. barium swallow) as being the first step. Can be done laparoscopically. * With most dysphagia. * Say you tried lifestyle modifications. You cannot make the diagnosis of achalasia without an esophageal motility study. Metoclopramide will not help tighten the LES because the LES is now replaced with collagen. Definitive procedure is a myotemy.50 - . If the wrap is too tight. Acetylcholine keeps LES shut at rest. The cause is likely esophageal motility problem. The most common cause is reflux. the fundus is wrapped around the LES so that the LES has a sleeve tightening it. some confusion in the elderly. the patient still has reflux. In scleroderma. thus metoclopramide can tighten the LES. * Manometry of diffuse esophageal spasm would show diffuse disordered peristalsis. So also do an endoscopy with biopsy when you see achalasia. You also see inappropriate contraction of the LES that does not relax. but the major side effect is torsades de pointes due to prolonged QT. So there is no peristaltic waves in the esophagus. Barium swallow will slow a DO NOT DISTRIBUTE . In this surgery. * 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. Maybe there is a cancer near the esophagus or there is a stricture. Another option is to inject the area near the LES with botulism toxin because that poisons the acetylcholine.Study Notes – Internal Medicine James Lamberg 28Jul2010 and are effective for most people. so they would relax the LES. So a patient with chest pain who got worse with nitroglycerine we would suspect GERD once cardiac is ruled-out. Dysphagia * 32yo woman with no past medical history comes to your office for evaluation of difficulty swallowing foods. Dopamine at the LES causes relaxation. Drugs like cimetidine or azithromycin could potentiate cisapride. When you do an upper GI series (i. added metoclopramide and the patient still has symptoms. Give large dose PPIs. * 30yo man with mid-chest pain has had several negative cardiac workups. * Treatment of achalasia is usually be pneumatic (balloon) dilation at the LES to tear the muscle fibers. Surgery should be considered after no relief from maximal medical therapy. * Cisapride is no longer available. but this does not work very well long-term. That pump is blocked by PPIs. The drug was pulled due to a fair number of sudden deaths. barium swallow). This is achalasia. * Nitrates and calcium channel blockers are smooth muscle relaxants. If not tight enough. She has had the problem for over a year and has trouble with solid foods. Lack of dopamine causes Parkinson-like symptoms.

He has esophageal cancer. * 75yo man comes to see you because he thinks he has bad breath. On physical exam. Pushing the food can break the ring too. and angular cheilosis. but the history is not progressive it is episodic. you can jump to the endoscopy to directly visualize the ring. but go with barium esophagram first. but that is adjunctive therapy.51 - . But. If the history is classis though. * Some evidence that squamous carcinoma responds to chemotherapy and radiation. He coughed up the chicken teriyaki that he ate two days earlier. * Treatment via endoscopy would be removal of stuck food or carefully pushing the food through the soft ring. We don’t know if this patient has squamous cell carcinoma or adenocarcinoma. major weight loss. This past weekend a most disturbing event occurred while he was watching a football game. the most common being colon cancer in the United States. The story is William Mayo (Mayo clinic) was a surgeon at the beginning of the 20th century. iron deficiency anemia. He has had no prior episodes except nine months ago he had a single similar episode that gradually resolved over several hours. no diagnostic test needed to tell us this.5cm left supraclavicular lymph node (Virchow node) but otherwise exam is normal. Food can sit there for some time but typical history is coughing food back up at the time of eating. The barium swallow is done first to help determine if you can get an endoscope through since there is a risk of perforation. Esophageal Cancer * Plummer-Vinson syndrome signs include upper esophageal web. more commonly seen in an older patient and associated with coughing and gurgling as soon as they start eating then spit it back up. The term nutcracker esophagus is used because the manometry peristaltic wave pressure can be so high it is said they can crack a nut. if you find the Virchow node you assume gastrointestinal cancer. What is the next step in the evaluation of this patient? * Can this be achalasia? Yes it can be. These peri-umbilical nodes are called Sister Mary Joseph nodules. * So 62yo guy with dysphagia. It is a risk factor for esophageal cancer. But most likely Zenker diverticulum. He complains of severe chest pain and feeling that food is stuck in the mid-chest. With these think of a gut cancer. Physical exam is normal. He has a medical history of significant reflux esophagitis for 15yrs and a 40pack-year smoking history. * Treatment of diffuse esophageal spasm is nitrates or calcium channel blockers to relax the smooth muscle. Other options include pneumatic dilation. Of course you do the diagnostic tests though prior to surgery. The cancer can be anywhere in the esophagus and it usually takes an irregular ulcerated pattern. He claims to brush his teeth every night. The gut lymphatics drain through the left supraclavicular node. He has had a 20lb weight loss. Schatzki ring thought to be due to chronic acid exposure. * 62yo man comes for evaluation of progressive difficulty swallowing solids and recently semi-solids for four months. Think cancer until proven otherwise. Barium x-ray would show an upper esophageal ring. The caliber or width of the ring is variable and in general it is soft mucosa.Study Notes – Internal Medicine James Lamberg 28Jul2010 corkscrew esophagus as there is diffuse non-ordered peristalsis. * Nodules in or around the umbilicus are also highly suggestive of gastrointestinal cancer. This often occurs in the setting of a tight UES. Then do the endoscope with biopsy. The Schatzki ring is always found just above the LES. Thus. * Diagnostic test is barium esophagram showing pocket. All the Mayo nurses at the time were nuns and Sister Mary Joseph did the surgery prep for Dr. * Zenker diverticulum most commonly at upper esophagus. also known as steakhouse syndrome. but it doesn’t really matter because surgery is the only hope for a cure. Work hard to rule-out cardiac causes of chest pain before you jump to the motility work-up. you find a 1. Barium x-ray would show a ring or band near the LES. but treatment is the same (surgery). Virchow node. almost always adenocarcinoma. * Most patients with esophageal carcinoma will give a history of smoking and/or alcohol use. Mayo’s patients. most things get through until you hit the critical diameter like a large piece of steak that does not get through. So what tests do you do? There is some controversy. DO NOT DISTRIBUTE . so not a fibrous piece of tissue. so they also get a surgical cricopharyngotomy (cricopharyngeal myotomy) of the UES. Think Plummer-Vinson when you see a low Hct and low MCV with upper esophageal issues. treatment is surgical diverticulectomy. * Nobody died of a little bit of esophageal spasm. meaning of all those that have gastrointestinal cancer only a few will have the Virchow node. He notices people tend to keep their distance from him because of this. Since then he has had no heartburn or weight loss. * There is no medical treatment for Zenker diverticulum. Biopsy important near the LES to distinguish squamous carcinoma from adenocarcinoma. * Primary treatment for any esophageal cancer is surgery. may show an apple-core lesion on barium swallow. * Virchow node is not common. * 40yo man presents to the ED after going to dinner. Once in a while she would feel the nodules in the umbilicus. * Episodic mechanical dysphagia (large bolus of food) should suggest a Schatzki ring. Squamous cancers along with head/neck cancers are associated with chronic alcohol use and smoking. squamous carcinoma since we are at the top of the esophagus.

if the patient has esophageal symptoms and thrush on their tongue it is fair to say the patient has esophageal thrush (candidiasis). Virology can show which grows out but viral cultures are unreliable. DO NOT DISTRIBUTE . a stimulant from antral cells. Anti-cholinergic drugs have poor side effects like dryness and urinary retention. HSV. They keep vomiting and red fluid starts coming up (blood). Gastrin is secreted and travels through body in bloodstream. and HIV-caused ulcer (least common) all of which are indistinguishable from each other. It is not from the HIV as the initial insult but due to the inflammation that the HIV causes. Pernicious Anemia * Chief role of the stomach is to grind food as only several millimeters can get through the pyrosis. you know the patient had candidiasis. or famciclovir. This is a Mallory-Weiss tear. * Thrush looks the same in the esophagus. a longitudinal mucosal tear (not full thickness). They keep vomiting and bile starts to come up (stomach empty). Intrinsic factor is not needed for subcutaneous B12 injections because that does not absorb via the GI tract. candida is usually in the upper third of the esophagus with small nodules. some need endoscopic treatment. * Common symptom of esophagitis is odynophagia. Rather than put the patient through endoscopy you can treat them with fluconazole. It is a complete horizontal full-thickness tear of the esophagus casing esophageal separation. There is no endoscopic determination that can be made visually to determine what kind of virus. * Boerhaave syndrome is also caused by retching and is much more rare. * Histamine stimulates the parietal cell and acetylcholine as well. The Gcells in the antrum secrete gastrin so removing the antrum (antrectomy) would eliminate another stimulus for acid secretion. * We have H2 blockers but no real drugs in clinical practice to block gastrin or acetylcholine at the parietal cell. Endoscopist can do various techniques to stop the bleeding at that point if required. gastrin) it does not matter because the whole cell output is blocked. Types that occur are CMV. Wait. white cottage cheese-like plaques. You can scrape the plaques off and put them on a slide (KOH prep) to see budding forms and hyphae. You won’t see infectious agents on barium x-ray. can be just dysphagia though. * Pernicious anemia is due to loss of parietal cells and thus loss of intrinsic factor. * With the exception of the HIV patient. Stomach makes pepsin. * Immunocompromise increases risk for infectious agents. * Intrinsic factor from parietal cells is essential for absorption of dietary B12. Parietal cell also secrets intrinsic factor for vitamin B12 absorption.52 - . Esophagitis * The most common cause of esophagitis is GERD. prednisone for an immunocompromised patient with an infection? Yes. in this particular incidence. CMV usually shows severe inflammation with large ulcers. However. Treat with fluconazole. This is life-threatening. * Most Mallory-Weiss tears resolve on their own. * Say the patient has no thrush or had thrush but still has esophageal symptoms a week later.Study Notes – Internal Medicine James Lamberg 28Jul2010 * Caustic ingestion especially with lye can lead to strictures. * Treatment for CMV esophagitis is ganciclovir or foscarnet. rarely steroids. * Esophagitis in HIV patient think endoscopy with biopsy. Over time the strictures can degenerate into squamous cell carcinoma. acetylcholine. which are the natural defenses against HCl. There are several types of infectious ulcers that can cause symptoms. Stomach also secretes gastrin. * Medical student goes out to celebrate passing USMLE Step 2 and drinks too much then begins to vomit up the steak that they ate. Intrinsic factor links with B12 and get absorbed in the terminal ileum. * Treatment for HSV esophagitis is acyclovir. 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. * Treatment for HIV-induced ulcer (diagnosis of exclusion) is prednisone. Give prednisone for a week and if symptoms disappear you have confirmatory evidence that it was HIV-induced ulcers. valacyclovir. leading to megaloblastic anemia. * Water and bicarbonate secreted in the stomach. * Biopsy will show cytomegalic cells and/or owl’s eye inclusions (CMV) or ground glass cells and/or Cowdry type A bodies (HSV). You’d lose parietal cells with a sub-total gastrectomy or patient has a large gastric tumor that gets removed. Next most common are infectious agents. HSV usually shows small discrete ulcers without plaques. so it plays a minor role in digestion of proteins. * Ulcer seen in esophagus and you want to determine what kind. * The benefit of PPIs is that no matter what the stimulation to the parietal cell (histamine. * Mallory-Weiss diagnosis is made by endoscopy seeing the lacerations. * Acetylcholine comes from nerves so a surgical vagotomy would eliminate one stimulus for acid secretion. so HIV. What is the next best test? Endoscopy. You can remove the stomach and do just fine with proteins though because the pancreas creates plenty of proteases. a protease. Vagotomy and antrectomy are not common anymore due to the prevalence of effective ulcer mediations. If symptoms relieve in 7 days. chemotherapy.

* There it lots of overlap between gastric and duodenal ulcer symptoms. but least expensive test. * With H. * COX-2 metabolites are leukotrienes. boring pain (meaning it feels like it is going to bore through you). creates an alkaline environment around itself to protect from HCl. * Neutrophils in pernicious anemia will be hypersegmented. which was the cause of rofecoxib being pulled off the market in 2004. tetracycline. pylori was once named campylobacter-like organism. does not differentiate current from past infection. Say you had a positive biopsy or breath test and you treat the patient. bleeding (could ulcerate into a vessel). then pick misoprostol. If asked what drug will reconstitute prostaglandin activity. * If patients has rheumatoid arthritis and ulcers. * CLO test is taking biopsy tissue from antrum and putting it in yellow gel. pylori is a Gram-negative organism that lives in the antrum of the stomach in the mucus bicarbonate layer. Ulcers * Typical symptoms of any ulcer is epigastric pain. They maintain good blood flow to the stomach and tight gap junctions. would also show sky high blood gastrin levels. So every patient with an ulcer should be tested for H. and has a number of actions leading to ulcer production (e.g. Least accurate test is blood IgG looking for antibody. COX-1 metabolites. naproxen.53 - . women can buy these medications to abort early in pregnancy (less efficacious later in pregnancy). * Never give misoprostol to pregnant women or even women of childbearing years. clarithromycin. do endoscopy with biopsy of the antrum and the pathologist will find H. pylori negative. Side effects are diarrhea and abdominal cramping. Prostaglandins increase intestinal motility and uterine motility. Called CLO because H. make tummy better. * Another regimen is MOC. is not very helpful. azithromycin. Mnemonic for -coxib drugs to remember COX2 is “-cox” and “b” for 2nd letter in alphabet. Urease will turn the yellow gel to pink. * Gastrinoma is a tumor comprised of gastrin cells. You do endoscopy and see ulcers. with or without nausea. there is over a 90% chance that the patient will develop another ulcer. gastric outlet obstruction symptoms (chronic scaring. Trying to distinguish the type of ulcer based on getting better or worse with food. penetrating (pancreatitis as ulcer bores into back). usually outside the stomach. which is very accurate. Non-specific cyclooxygenase (COX) inhibition is seen with older NSAIDs like ibuprofen. Misoprostol is part of a home abortion kit. think peptic ulcer disease. you’d want to go with the COX-2 inhibitors. * H. is infection with Helicobacter pylori. * Mnemonic: MTB. pylori has many regimens. pylori. * If you treat an ulcer but not H. The gastrin-secreting cells are autonomous (not shut off by acid section). In countries where abortion is legal. a negative feedback loop. Zollinger-Ellison syndrome. omeprazole. Methotrexate is used to kill the fetus and misoprostol is used to evacuate the fetus. stimulates meal-induced gastrin). perforation (surgical emergency). pylori.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. Proton pump inhibitors are useful too. * Intrinsic factor from parietal cells goes back and shuts down gastrin. metronidazole. If patient has NSAID-induced ulcer. COX-2 specific medications have been association with vascular events. relation to food (might be improved or worsened). It is not an invasive organism. Bismuth also has bactericidal effects. It is specifically designed to defeat the problem of NSAIDs. and asprin. look for anti-parietal cell antibodies and anti-intrinsic factor antibodies. * The vast majority of community acquired ulcers. tetracycline. pylori on the surface of the antrum. Always use at least two antibiotics. gnawing pain. * Pain that is better with eating and then gets worse. gastric or duodenal. * Non-invasive tests for H. metronidazole. DO NOT DISTRIBUTE . this is a black box warning. Normal is < 50 blood gastrin. Could be folate or B12. patient on PPI might be 80-100. then stop NSAIDs and try to make the ulcers better. * NSAIDs come in COX1 and COX2. * Ulcer complications include pain. cytotoxic. namely prostaglandins and prostacyclin. in non-ICU patients who are not taking steroids or drinking alcohol. amoxicillin. It secretes urease. pylori include metronidazole. are important in the cytoprotection of the stomach. * Misoprostol is an analog of prostaglandin. ulcers are most likely due to NSAIDs. and some label it as COX-3 (but COX-3 does not have anti-pyretic properties). sometimes three. we use PPIs. So with no acid. * Bactericidal antibiotics for H. clarithromycin. So being more specific with COX2 blocking will help relieve aches and pains but not block the prostaglandins that are important for gastric protection. Although there is come controversy on acetaminophen as it does not exhibit anti-inflammatory properties. the gastrin goes high to 1000 range. * Biopsy of patient with pernicious anemia would show atrophic gastritis. remember you never use a single drug because resistance becomes problematic very quickly. To determine if you treated the patient accurately you can check a repeat breath test or stool antigen test. repeated ulcers). COX-2 inhibitors include celecoxib and acetaminophen. bismuth. pylori include breath tests to measure for exhaled urease. * Treatment for H. Classic symptom is nocturnal epigastric pain that wakes someone from sleep.

often microscopic. pylori is present in patients with gastric ulcers and duodenal ulcers. * Erythromycin is the next option because it stimulates motilin receptors. If the food just stays in your stomach for 8 hours. * Think gastrinoma when you see diarrhea with multiple ulcers. 2 hours later when the regular insulin works the patient has a period of hypoglycemia. problem-specific treatment is misoprostol. * Cisapride no longer used due to increased QT interval leading to torsades de pointes. Some of the tumors can be microscopic and you can have metastatic Zollinger-Ellison syndrome rarely. In normal people. Gamma counter put over patient to see how long food sits in the stomach. * 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. * H. they feel gassy and bloated. What would cause this? An autonomous constant drive to secrete gastrin. * What if you can’t take the tumor out? Do we have a drug that reduces gastrin? Not currently. associated with gastric adenocarcinoma as well as gastric lymphoma. Gastroparesis * The majority of gastroparesis cases are seen in diabetic patients. pneumoperitoneum on x-ray. With gastrinoma there is no feedback inhibition so serum gastrin is in the hundreds or thousands. then you inject secretin via IV. are usually found in the head of the pancreas or region of the common bile duct and usually not found in the stomach. You would get a prolonged gastric emptying test with gastroparesis or a mechanical obstruction like a tumor pushing up against the gastric outlet. do an imaging study like a CT scan looking for the tumor. We do have a drug that suppresses acid so use that. use COX-2 in future. Physical exam is unrevealing. Side-effect is dopamine inhibition and therefore Parkinson-like symptoms like bradykinesia. free air under the diaphragm. * Once high serum gastrin is confirmed by secretin stimulation test. * This can be a particularly difficult problems for diabetics because they time their insulin doses with eating. Gastrinoma (Zollinger-Ellison Syndrome) * 42yo woman comes to your office with complaints of diarrhea for six months. to confirm you are not dealing with a mechanical obstruction. The motilin receptor in the stomach responsible for peristalsis gets activated because erythromycin simulates the motilin hormone. * The diarrhea is due to the acid spilling out into the pancreatic area. Her past medical history includes peptic ulcer disease for many years that has been relatively resistant to medical treatment. Secretin is released by the small bowel to cut down acid production by causing water and bicarbonate production. a gastrinoma. * Gastrinoma tumors. the food hits the small bowel and the patient gets hyperglycemia. * Why hypercalcemia? MEN-1 syndrome associated with parathyroid tumor. * Test to order is a serum gastrin level. Patient eats a meal mixed with nuclear chemical. If you give secretin IV and gastrin level increases. * There is damage to the neural innervation of the stomach. biopsy to determine if benign cause versus malignant cause like adenocarcinoma. What is your next step in evaluation of this patient. whether x-ray or endoscopy. * Mucosa associated lymphoid tissue (MALT) is a localized lymphoma. If you can find the tumor. feel progressively uncomfortable throughout the day. 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. Treat patient with multiple antibiotic regimen for about 14 days. Then when the insulin wears off. * NSAID-induced ulcers treated with PPIs. Wouldn’t omeprazole increase serum gastrin level? Yes. * Most important thing to ask in a patient with an ulcer is does this patient have Helicobacter. take it out. causing hypercalcemia. * Test is nuclear gastric emptying scan. or other ulcer problems * The patient still has ulcers even at maximal PPI therapy. may ultimately need to vomit to relieve the symptoms. * Antacids may be used in addition to the other medications for ulcer symptom relief. * Look for other signs of neuropathy like autonomic dysfunction (orthostatic). secretin inhibits gastrin production so you see a fall in serum gastrin. which inactivates the pancreatic enzymes and there is ineffective digestion. * Treatment includes metoclopramide to improve gastric motility. massive doses of PPIs. Lab results are normal except for mild hypercalcemia. The goal of timing is to match when the carbohydrates are digested in the small bowel mucosa. peritoneal signs. think Zollinger-Ellison syndrome. * Signs of gastroparesis are feeling full very quickly after eating. about 5% are gastric lymphomas. usually Type 1 diabetes. Obstructing lesion would show scaring and inflammation from the ulcer on endoscopy. there is always an association with DO NOT DISTRIBUTE . There has been no improvement in symptoms. You have to do some test. but not to the 100s range with a PPI. bad history of ulcers. She takes maximum doses of omeprazole daily along with famotidine and still has symptoms. 95% of cancers in the stomach are adenocarcinoma. which is important for peristalsis.54 - .Study Notes – Internal Medicine James Lamberg 28Jul2010 * Perforation would present as an acute abdomen.

it is a stool packaging factor. Rule out infectious etiology before labeling them with this life-long disease. If just the rectum. but not mesalamine. anti-spasmotics for cramping pain. so a reversible side effect. Another name for 5-ASA is mesalamine or mesalazine. next step is steroids (oral or rectal). * Crohn disease symptoms are abdominal pain usually RLQ. some weight loss. Biopsy will show mucosal inflammation. no anti-platelet action). which is always present in MALT. usually presents as a younger women (teens. or more commonly alternating diarrhea/constipation). showing cobblestone pattern. No fevers. * IBS thought to be due to altered motility in the bowel. symptoms include combination of crampy abdominal pain associated with altered bowel habits (diarrhea. IBS is not associated with any inflammatory signs or symptoms. UC affects the mucosal layer only. no elevated sedimentation rate. * Irritable bowel syndrome (IBS) is far more common than any other bowel condition. specifically Ashkenazi Jews. Bloody diarrhea for a few days is more likely to be infectious colitis. Inflammatory Bowel Disease (IBD) * Inflammatory bowel disease (IBD) covers Crohn disease and ulcerative colitis (UC). etc. Disease to the splenic flexure. it is proctitis. the anus is not involved. * Treatment for IBS is symptomatic as well. * By definition. 20s. About a liter a day leaves the ileum and enters the cecum. So you have ruled out inflammatory diseases when you diagnose IBS. protosigmoiditis. so anti-diarrheal agents if needed. Her medical history is negative but he has ulcerative colitis.55 - . The “nervous stomach” people get before big exams is sort of an irritable bowel symptom. Although 5-ASA looks like aspirin. no organomegaly. If that fails. * Job of the colon is to absorb water. * Say patient is not improving with sulfasalazine or mesalamine. nausea. 30s). no weight loss. Full body workup for lymphoma is negative. diarrhea. * Any ethnic group can have Crohn disease. constipation. Sulfasalazine may be the cause. Once medical therapy fails. * Mesalamine can be given as an enema or suppository as well * Sulfasalazine. After stopping the medication sperm counts will return to normal. * Crohn disease can affect the colon but specifically there will be terminal ileum involvement. no night sweats. no matter DO NOT DISTRIBUTE . Crohn is transmural through the full thickness of the bowel wall. * Treatment of UC is sulfasalazine and steroids. Y. More of a vague non-specific exam. aggressive doctors may use cyclosporin. Crohn occurs in patches. 32yo woman visits due to problems with fertility. pylori treatment without chemotherapy. If rectum and sigmoid.g. Sulfasalazine is sulfa connected to 5-ASA. no nocturnal diarrhea. * IBS treatment is to increase dietary fibers. * Acute terminal ileitis associated with Yersinia enterocolitica. higher incidence in Jewish particularly of Eastern European origin. pancolitis. * UC occurs over weeks to months. vomiting. stool softeners or laxatives as needed. These patients can sometimes be cured with plain H. If colon is ulcerated and inflamed. bloody diarrhea. If that fails. it has none of those effects (no anti-inflammatory outside the gut. Entire colon. * Patient gets endoscopy and lymphoid tissue is found in the stomach (MALT). negative stool studies will help rule out infectious agents. so colon absorbs about 85% of the water giving you 150mL of liquid in the stool. look for bowel irritants like food and stress. Many patients with Crohn disease will have a relative with the disease. admit for IV steroids. skip lesions. * Ulcerative colitis starts at the distal rectum right above the anus in the columnar mucosa. * Test for UC can be done on the first visit via a flexible sigmoidoscopy. not guaiac positive (unless they have hemorrhoids from straining if constipated). is called a syndrome because there is nothing we can point to that looks inflamed or abnormal. it cannot do its job so you get diarrhea and blood. radiation. enterocolitica is the most common contaminant of stored blood and can live at lower temperatures (e. So look for terminal ileum inflammation. terminal ileitis.Study Notes – Internal Medicine James Lamberg 28Jul2010 Helicobacter. * UC never involves the ileum and is always continuous. refrigerator). showing lead pipe pattern. * In IBS. maybe altered sensitivity to pain sensation in the intestines. or rare photosensitivity. Yersinia is siderophilic (iron-loving) so patients with hereditary hemochromatosis are more susceptible. blood counts are good. You want to see the whole colon so do a colonoscopy. Treatment is antibiotics. no peritoneal signs. there is symmetric circumferential continuous disease for some portion of the colon. Diarrhea can be bloody but more typically is non-bloody diarrhea. What do you do? Answer is treat H. no mucus or pus in stool. left sided colitis. or surgery. Side effects of sulfasalazine tend to come from the sulfa portion. * Crohn disease is also a chronic disease but unlike UC. whether it is sulfa intolerance with headaches. affects the sperm count and sperm motility. May occur with other syndromes that have vague symptoms like fibromyalgia or chronic fatigue syndrome. the patient will not have focal findings. Older patient for a few days it might be ischemic colitis causing bloody diarrhea. or rare hemolytic anemia. no anemia of chronic disease. pylori.

These usually correlate with the underlying irritable bowel disease. Entamoeba is a parasite typically in the ileum or colon. pyoderma gangrenosum). Vibrio cholera) watery diarrhea without mucus or pus or blood or fever. gastrin. emerging to the perianal area or buttocks draining mucus. and primary sclerosing cholangitis (sclerosis/fibrosis of the bile duct. entamoeba histolytica. typically traveling. ETEC E. disulfiram-like reaction with alcohol causing bad nausea/vomiting (rare but serious). Infliximab also approved in rheumatoid arthritis. remove the entire colon. Infliximab not needed every day. * All of these diagnoses are made by stool studies. this is different than regular adenocarcinoma where you do a segmental resection. Unlike in UC. So if the patient has a lot of ileum involved and maybe jejunum. the sulfasalazine link of sulfa to 5-ASA is cleaved at the distal ileum making the 5-ASA (mesalamine) available at the proximal colon. Inflammation can occur in anal crypts and burrow through the soft tissues. * Enteroinvasive invade the mucosa (shigella. * Campylobacter jejuni is one of the most common causes of enteritis. Salmonella can be enterotoxic in one form. It is a monoclonal antibody (-mab) against tumor necrosis factor (TNF-alpha).g. Saint Petersburg Russia. gas. Infectious Colitis * Infectious diarrhea occurs in enterotoxic and enteroinvasive. Enterotoxic E. Side effect of metronidazole is upper GI discomfort (nausea). coli or cholera are secretory forms of diarrhea. * Perianal fistulas can occur in Crohn disease. * TMP-SMX works for most bacteria and quinolones work for nearly all causes of enterotoxic or enteroinvasive bacterial diarrhea. coli.56 - . The specific antibiotic for perianal fistula is metronidazole. Treat with fluids. * Extra-intestinal manifestations of IBD include arthritis (e. maybe hiking or drinking from a stream. iritis). sacroiliitis. Look for narrowing. cobblestone appearance (more intense ulceration). * Secretagogue is something that causes secretion. For entamoeba. Similar to Barrett esophagus. eye involvement (uveitis. Low grade dysplasia is treated by treating UC and seeing if it goes away. mouth ulcers (aphthous ulcers). vomiting. coli O:157 (EHEC). particularly UC in the colon. next step is total proctocolectomy. * IBD. Do an upper GI series with barium then give extra barium to get to distal ileum. such as a toxin.Study Notes – Internal Medicine James Lamberg 28Jul2010 how much of the colon is affected by UC. 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. * Patient has blood diarrhea. Secretory & Osmotic Diarrhea * Secretory diarrhea means there is some secretory drive for the intestine to put out lots of water. straight/flat back). serum creatinine is 2. Surgery also for complications of Crohn like progressive small bowel obstruction or perforation or bad fistulizing disease with abscesses. However. ulceration. * Diagnostic test for Crohn disease is upper GI series with small bowel follow through. pus. skin involvement (erythema nodosum typically on lower extremity. Symptoms are belching. maybe once every few weeks depending on patient. use mesalamine alone because it is generally released higher up in the intestinal tract. Shigella dysentery has typical blood and pus in stool. headaches. VIPoma (vasoactive intestinal peptide). metallic taste. increases the risk of cancer. after 10 years of UC disease in the colon the patient requires colonoscopy surveillance to see if the patient is developing dysplasia. proximal jejunum). remove the entire colon. If cancer. Side effects include a lupus-like drug reaction with antihistone antibodies. With UC cancer you remove the entire colon. and/or stool. ETEC is the most common cause of traveler’s diarrhea. foul smelling stools. Mnemonic: infliximab inflicts pain on TNF. * Failed medical therapy in Crohn should go to surgery. reactive arthritis of small joints). Next step is steroids after mesalamine and antibiotics. DO NOT DISTRIBUTE . remove entire colon. do rectal parasite testing looking for ova or protozoa. nausea. campylobacter) bloody diarrhea with fecal leukocytes and fever. * Crohn disease is treated similarly. looks ill. you try to take out as little bowel as possible with Crohn disease. acute onset. give IV infliximab. treat with quinolones or erythromycin. High grade dysplasia is confirmed by a second pathologist and treated like cancer. coli can respond to antibiotics like TMP-SMX or quinolones. * Enterotoxic (E.5. hematocrit is at 19%. hemoglobin is 6 grams. Far more commonly in Crohn is a localized ileal resection. * Extra-intestinal manifestations of IBD that do not follow the condition of the underlying bowel disease include ankylosing spondylitis (bamboo spine. numbness/tingling due to peripheral neuropathy. This is hemolytic uremic syndrome associated with E. Treatment of giardia is metronidazole. * Yersinia enterocolitica can mimic Crohn disease or appendicitis. * Giardia is a parasite that lives in upper intestine (duodenum. diarrhea. * If severe fistula disease not better with metronidazole or severe Crohn disease not getting better with medical treatment. young men typically present with jaundice and itching).

campylobacter in the hospital. Also cephalosporins or penicillins because we use those medications more than clindamycin. If very sick patient. Add stool to plate. 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. do a toxin assay. given oral. terrible neuropathy) use vancomycin. patient is taking laxatives. * Pseudomembranous colitis associated with a very high white count (e.Study Notes – Internal Medicine James Lamberg 28Jul2010 calcitonin. * In clinical practice. * Say you measure 2*(Na + K) as 274 and osmolarity is 350.000). With lactase deficiency. antibiotics as a side-effect. * Patient do not develop shigella. There are also strains of vancomycin-resistant staphylococcus. difficile patients do not have sky-high white counts.57 - . milk sugar. You’ve done all the studies and hormone assays but found nothing.g. This appearance does not look like anything else so you can tell the patient right there that they have pseudomembranous colitis. In a negative sigmoidoscopy. nurse). gut tries to dilute non-absorbable lactose. you can differentiate osmotic from secretory diarrhea from clinical presentation and initial laboratory testing. they don’t want to wait for a few days they want to know now so get your sigmoidoscope and get moving. * Ways to get C. appendectomy. probably secretory. or being exposed to diarrhea (nosocomial infection). difficile does not grow in the gut but when you wipe out the normal flora with antibiotics the C. difficile. which are yellow exudative plaques on the colon. colchicine. go for sigmoidoscopy. usually non-bloody. but not all patients with C. difficile colitis includes clindamycin (most likely). Patient may have multiple operations that they don’t have good reason for. difficile are being in a hospitalized/nursing home setting. Normally C. * Direct way to make the diagnosis would be to put a sigmoidoscope in the patient and look for pseudomembranes. etc. gold salts for rheumatoid disease. salmonella. There are also strains of VRE (vancomycin-resistant enterococcus) “superbugs” so metronidazole is first-line. * Osmotic diarrhea means there is an osmolar substance that is not absorbed in the small intestine. so gap of 76mosm of something that does not belong there. Vancomycin is more expensive than metronidazole. He has had diarrhea for the past 5 days. Medication causes include magnesiumcontaining drugs. C. like cholecystectomy for vague symptoms. receiving antibiotics. What is your next step in the evaluation of this patient? * Top of the differential list should be pseudomembranous colitis (C. Enterocytes have villi and microvilli with lactase enzyme. Think factitious diarrhea. So besides the Na+ and K+ there is nothing else that has osmolar properties in the stool. difficile. * Most common osmotic agent is lactose. * Young female patient has supposed secretory diarrhea. so look at medication list for antibiotics. Patient may have connection to the medical field (works in drug store. difficile. Next step is vancomycin. Exam shows vague mile left mid-abdominal pain. * Stool Osmolar Gap is a calculation you will probably only see on the boards. if cytotoxic then we know it is coming from C. Ischemic Colitis * 72yo man complains of LLQ pain for the past few days. Stop antibiotics in these cases. paramedic. * Antibiotic-associated colitis (non-pseudomembranous) is diarrhea associated with the change in flora that occurs with antibiotic use. * Treatment is metronidazole first-line. * 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. Patient in the hospital is likely nosocomial or medications. To get stool osmolality 2*(Na + K) so 274 here. close to 274. stools bloody DO NOT DISTRIBUTE . He is treated for 7 days with IV cefazolin with dramatic improvement in his symptoms. difficile colitis). PO (oral) is very effective. difficile so hand-washing with soap and running water is required. Alcohol-based hand sanitizers do not remove C. If not very sick. Say it is 275. but if it is present it points you to C. even if you’re a gastroenterologist. diff can start to flourish. quinidine. and even that is not perfect because the spores are so sticky. WBC of 30-50. So not likely osmotic diarrhea. can wait for toxin assay. colonic (left sided abdominal tenderness). diff lives in the lumen of the gut so you want to clear it from the lumen of the gut. * Everyone with pseudomembranes on exam has C. * Causes of C. * Now measure osmolality directly for the stool. so the small intestine tries to dilute it by adding water into the lumen of the small bowel. * C. * Most C.g. spectrum from well with mild diarrhea to very toxic-appearing with high fevers. difficile causes a secretory diarrhea. 3 exploratory laparotomy operations. so this is an osmotic diarrhea. * If patient cannot tolerate metronidazole (e. Bacteria can ferment the lactose so patient can get a lot of gas and discomfort as well. IV metronidazole gets into blood stream but not really to lumen of the gut. Pseudomembranous Colitis * 59yo construction worker is admitted to the hospital for treatment of cellulitis that developed after dropping a steel beam on his leg. difficile make pseudomembranes. You may get called to the ICU for a very sick patient who has been on many antibiotics.

* Fat soluble vitamins are “in the attic”: A. patients generally get better. * Patient may have fever.e. * Protein malabsorption signs are hypoalbuminemia and peripheral edema. superior pancreaticoduodenal. Exam shows some tenderness. horrible central abdominal pain. where the hypogastric or internal iliac artery takes over. * Mnemonic is FIC for folate. and IMA. * Losing the SMA would infarct the entire small intestine. Vitamin K deficiency measured by protime (PT) or INR. like celiac sprue. K. * Symptoms include weight loss.58 - .g. * Malabsorption is an osmotic diarrhea. high RDW). calcium. Patient may show signs of calcium deficiency like osteopenia or tetany (Chvostek or Trousseau sign). do an abdominal aortic angiogram. * If proximal small bowel is affected alone. The patient is writhing around as if they have a perforation. diltiazem. SMA. * SMA ischemia risk factors include atherosclerotic heart disease. osteopenia/osteoporosis with no reason (e. Less likely is ischemia. digoxin use. metformin. * Vitamin A deficiency will show disturbances in night vision and hyperkeratosis. rectal exam reveals bloody stool. History is significant for peripheral vascular disease and a myocardial infarction. What vessel is most likely involved? Inferior mesenteric artery (IMA) serving distal transverse colon to midrectum. leukocytosis. Other thing on the list is infectious colitis. acidosis (lactic acidosis from poor perfusion). Vitamin E deficiency (rare) will show nystagmus and ataxia. splenic. Vitamin D deficiency will show hypocalcemia. Patient might have both so the MCV might be normal but the width spread would be high (high RDW or RBC distribution width). get better with medical management. but now feels sick again (honeymoon period). propranolol. D. * If SMA ischemia is suspected. Vitamin K deficiency will show problems with clotting factors II.g. What is the most likely diagnosis? Answer is ischemic colitis. Presents again as an adult. factor VII has the shortest half-life * Three things if not absorbed in proximal ileum are not well compensated for are folate. healthy young man. You would probably die from the gangrene and if you did survive you’d have to be on IV feedings forever. but here we’re talking about malabsorption as the presenting symptom. nonspecific pain. * Ischemic bowel is a useless description since SMA and IMA ischemia are very different presentations. * Most things absorbed past the ligament of Treitz. atrial fibrillation). but abdominal exam is soft without guarding. History might be use of oral contraceptives. * If IMA is lost.Study Notes – Internal Medicine James Lamberg 28Jul2010 over last 48 hours. middle colic. Patient is on isosorbide dinitrate. * Pathophysiology of celiac sprue is autoimmune disease with destruction of villi showing villous atrophy with DO NOT DISTRIBUTE . aspirin. * Celiac sprue is the most common cause of chronic malabsorption. iron. premenopausal woman). greasy or fatty looking stool. and calcium. and has developed a temperature. 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). SMA feeds intestinal. elderly patient with atherosclerotic disease. This is the preperforation pre-gangrene stage. * Treatment is usually medical for IMA ischemia. diarrhea. Malabsorption Syndromes * Lots of diseases can cause malabsorption. Other major cause is tropical sprue. * Young patient with acute onset of diarrhea is most likely infectious. needs angiogram then surgery. where the superior mesenteric artery (SMA) stops sending branches and IMA starts sending branches. IX. and X. Less common (very rare) is Whipple disease. or pulmonary embolism at one point. patient would have to be hypercoagulable since they likely do not have atherosclerotic disease. * Three major gut branches off the aorta are the celiac. or other hypercoagulable event with no risk factors. glipizide. you see the localized or segmental colitis in the distal colon and sigmoid. IMA has bloody diarrhea. right colic. Things absorbed only at the terminal ileum are B12 linked to intrinsic factor and bile salts. patient may say they had to watch their diet as a kid and get food from special bakeries. bad CHF with poor flow. so the malabsorbed material will be from the small intestine. go straight to surgery. * Anisocytosis is the term used for mixed RBC widths (i. irregular heart rhythm that puts patient at risk for thrombi (e. * SMA ischemia symptoms are centrally located abdominal pain that is out of proportion to physical exam. patient will have signs of FIC deficiency like megaloblastic anemia (folate deficiency) or hypochromic microcytic anemia (iron deficiency). hypercoagulability (less likely). If ischemia is present and severe. SMA has usually non-bloody diarrhea. increased food consumption. * Ischemic colitis should be at the top of your list in an elderly patient developing acute bloody diarrhea. hepatic. malodorous stool (due to fat). * Celiac sprue typically presents in childhood with malabsorption. negative stool studies. Celiac feeds gastric. ileocolic. * The small intestine does the absorption. E. Where is the watershed area? At the splenic flexure. iron. VII.

elastase. 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. Example would be CNS involvement (dementia). and rye. lymphadenopathy. fluoroquinolone. hematochezia). * Whipple disease diagnosis confirmed on small bowel biopsy showing PAS-positive macrophages. The patient would put lots of fat into the 72h stool collection. Tell patient to eat a diet with a lot of fat (100g/day) and collect the stinking steatorrhea stool and go to the lab. no D-xylose in blood. Also anti-gliadin antibodies seen in sprue. proteolytic enzymes like trypsin. * A viral gastroenteritis can wipe out the villi for a few days but they come back in a week or so. you should have less than 7g/day of fat in the stool. look for anti-endomysial (most sensitive. * Diverticuli can rupture or perforate. Could also do a 5h urine collection (D-xylose in urine if normal. tetracycline. and no bleeding. * Treatment for Whipple disease is broad-spectrum antibiotics like metronidazole. tetracycline. where B12 is absorbed. cardiac involvement. fluoroquinolones.Study Notes – Internal Medicine James Lamberg 28Jul2010 blunting or complete loss of villi showing crypt hyperplasia. Small bowel absorption in chronic pancreatitis would be normal. * Treatment is broad antibiotics like metronidazole. they present with sudden painless bright red blood per rectum (BRBPR. Celiac sprue patients also get megaloblastic anemia but that is due to folate. * Diverticular spasm due to contraction against hard stools can cause pain. Say you see 50g/day then the patient is malabsorbing fat. X-ray plain film can show calcifications across the midline where the pancreas sits. joint involvement. If the rupture is well contained you can see bowel wall thickening on CT scan. * Definitive diagnosis is based on small bowel biopsy. DO NOT DISTRIBUTE . Gliadin is a property of wheat. * Whipple disease presents as malabsorption symptoms plus other organ involvement. This prevent the malabsorption and the long-term complication including intestinal lymphoma and intestinal adenocarcinoma. and fat digesting enzymes like lipase. also known as antitransglutaminase (tGT). Even on a high fat diet. * D-xylose depends on nothing except an intact small bowel.59 - . this is pathognomonic for chronic pancreatitis. More likely to get this done at home. older test and less specific. * Testing for malabsorption in general includes the 72h fecal fat collection. But patient does not get better on gliadin-free diet and no anti-villi antibodies. If normal absorption. tenderness. If bad perforation. If not well contained you can see abscess in the wall of the colon (intramural abscess) or more severe pericolonic abscess. This is exocrine insufficiency of the pancreas. So the diagnosis of sprue is not made from villous atrophy alone. where it gets weighted for large volume then measured for fat. spilling fecal contents out. Tropheryma whipplei bacteria can be seen on electron microscopy. There will be inflammatory cell infiltration such as lymphocytes. D-xylose is a sweet tasting sugar that does not appear in the regular diet. no D-xylose in urine if malabsorption). no villi. inflammation. Asia) who comes back and now has malabsorptive symptoms. 50g of D-xylose powder is added to water and patient drinks it. Patient presents with brisk arterial bleed. So these patients will have B12 deficiency showing megaloblastic anemia. 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. * Tropical sprue affect patients in the tropics (Caribbean. fever. LLQ findings on an exam even looking like a left-sided appendicitis (appendix is just a diverticulum on the right side). * Major enzyme classes all come from pancreas: amylase to digest carbohydrates. * Diverticular bleeding can occur in the dome of the diverticuli. It looks like celiac sprue if you were to do a small bowel biopsy. leukocytosis. * Tropical sprue affects distal small bowel. localized rebound. pressure against pipe wall). LLQ post-prandial pain that resolves after bowel movements. there will be D-xylose above a certain level in bloodstream. This causes diverticulitis. After removing gliadin from diet the villi grow back. * Most people over the age of 60 have diverticulosis but they are asymptomatic in general. India. Some patients can’t tolerate oats either. chemotropism. specific). barley. * Treatment is follow non-gliadin diet. you need the clinical features too. There is no need for active transport or breakdown by digestive enzymes. the diverticuli don’t bleed to give iron deficiency anemia or guaiac positive stool. skin involvement (hyperpigmentation). * Most common disease causing insufficient pancreatic enzymes is chronic alcoholic pancreatitis. * Test for small bowel absorption is the D-xylose test. plasma cells. LLQ pain of relatively acute onset. * Celiac sprue antibodies are against villi. If no absorption. * Diverticulitis is usually in an older patient. patient gets fecal peritonitis and will be very sick. blood measured 2h later. If you do a colonoscopy and see the diverticuli just leave them alone as long as patient is asymptomatic. Treat with high fiber diets to make stools bulkier giving some symptomatic relief.

Fluoroquinolones used as well. tumors of papilla of Vader. start IV antibiotics and go to surgery to clean up mess and resect area that is perforated. * Do not do endoscopy or barium/air enema with suspected diverticulitis because you can worsen the perforation. extensive Crohn disease. metronidazole. The baby is squeezing to empty their bowel and over time the more proximal bowel gets dilated. With mammography we hope to detect early cancer. * If patient not too sick. third is colorectal cancer. no fever. pancreatic cancer. worry about Hirschsprung. adenomatous polyps. * Peutz-Jegher is non-adenomatous polyps. * Older patient with acute change in bowel habits (constipation) think colon cancer until proven otherwise. change in bowel habits (constipation). DO NOT DISTRIBUTE . * Most common cause of cancer is men is lung cancer. bone tumors. PSA or prostate biopsies are not pre-cursor lesions. everyone should get a barium enema and flexible sigmoidoscopy at age 50.Study Notes – Internal Medicine James Lamberg 28Jul2010 * Diverticulitis is a localized perforation with abscess and no bleeding. In colorectal cancer we are finding a truly premalignant condition that we can remove and eliminate the cancer risk.60 - . ulcerative colitis. * Regular constipation can be treated with increased fiber and laxatives. * The premalignant condition for colon cancer is the adenomatous polyp. not adenomas. but you cannot miss this diagnosis. * Gardner syndrome is large bowel cancer with non-colonic involvement. * Screening tests can change over time. but it is still cancer. Gentamycin not used much. * Hirschsprung disease is a congenital loss of the myenteric plexus and the internal anal sphincter fails to relax. Colorectal cancer is second most common in non-smoking women and third most common in all women. * Most common cause of cancer in women is lung cancer. Do not confuse this with diverticular bleeding presenting with hematochezia. * Hirschsprung disease is rare in children and even more rare in adults. Better measurement would be too few bowel movements and bowel movements that are too hard. soft tissue tumors. Here we are discussing diseases that present with constipation as the primary symptom. we treat with IV antibiotics effective against anaerobes and gram-negatives like ampicillin. * Risk factors for sporadic colorectal cancer include Western diet (low fiber. * Diverticulitis diagnostic test is CT scan. abdominal pain. autosomal dominant). iron deficiency anemia (might be first symptom). Diverticulosis can be sigmoidoscopy. hyperpigmentation around lip corners. ovarian cancer). Occult blood with guaiac testing should occur annual beginning at age 50. BPH is not a pre-cursor. autosomal dominant. Rule-out hemorrhoids then maybe CT scan if cannot do sigmoidoscopy. In lung cancer. desmoid tumors. osteomas of the skull. Even now your screening could depend on what organization’s recommendations you follow. * The only preventable cancer of those top three is colorectal cancer. These patients get early colorectal cancer screening. high red meat). and third-generation cephalosporin. * Everyone should have an annual digital rectal examination beginning at age 40. * Test of choice if you suspect colorectal cancer is colonoscopy. * Older patient with blood in the stool. it depends on the patient’s normal daily bowel movements. * If family history is strong with adenocarcinomas. We could eliminate colorectal cancer (except familial forms) if we removed every adenomatous polyp in this country. Patients develop colorectal neoplasms at a younger age and with a higher likelihood. Constipation is a broad workup however. Specific genetic defect. think about hereditary non-polyposis cancer syndromes. non-polyposis familial cancer syndromes (Lynch syndrome. we find the cancer not the precancer. * Juvenile polyposis syndromes are also hamartomas. Treatment is surgery. Diagnosis is confirmed with full-thickness biopsy of rectum showing loss of myenteric plexus. Most recommendations say colonoscopy at age 50 for everyone because it is more sensitive and allows you to manage the polyps that you find. thin caliber stools (“pencil thin”). family history of colorectal cancer. At the least. * If diffuse peritonitis. they are hamartomas. no leukocytosis. Do most of those patients actually have colon cancer? No. Prostate cancer is next. * Any older person with iron deficiency has colon cancer until proven otherwise. * Diagnostic test for Hirschsprung is barium enema showing dilatation of colon above tight contracted sphincter. hereditary polyposis syndromes (familial polyposis coli. breast cancer. With severe constipation though. Chagas can also cause cardiomyopathy and myocarditis. but it might be difficult to see when blood is coming at you. Constipation & Colorectal Cancer * Constipation is defined as less than three bowel movements in a week. Early screening if family history. * Chagas disease (Trypanosoma cruzi) can cause megacolon and achalasia pattern due to loss of myenteric plexus from acetylcholine fibers. distention (if well advanced). generally resected. Breast cancer is most common in non-smoking women and second most common in all women. You can remove polyps and biopsy any mass. 90% or more of colorectal cancer is sporadic where the only history is polyps and/or first degree relative with polyps or colorectal cancer. Constipation in children is most commonly caused by regular constipation.

* Duke A cancer is limited to the mucosa. Beyond the duodenal bulb acid is neutralized so you do not get ulcers there. * Duke C is the staging that has increased survival with chemotherapy. * Presentation can be coffee ground emesis (blood). particularly seen in homosexual men with HIV. hematemesis. black tarry foulsmelling stool). * Polyp seen on colonoscopy can be sessile (broad base on wall) or pedunculated (on a stalk). Interval is controversial. Leucovorin is used as adjuvant therapy working synergistically with 5-FU. and even hematochezia since blood is a GI irritant and would have rapid GI transit. * First step in management of active GI bleeding is start large bore IV and give volume. say 3-5 years if small polyp. C1 means not full thickness and with lymph nodes. Layers are mucosa. * Chemotherapy drugs for colorectal neoplasm are 5-fluorouracil (5-FU) and leucovorin (folinic acid) or levamisole. Most upper GI bleeds are near the esophagus. Gastrointestinal Bleeding * Upper GI bleeding means the bleeding is originating from proximal to the ligament of Treitz. B1 means not full thickness. Duke D patient is too late. do not call it tubular because it looks like it has a tube. the muscularis mucosa. * If biopsy of a polyp (polyp not removed) and it is adenoma then you need to go back and complete the polypectomy. either pre-op or post-op to improve long term survival. which is the junction of the duodenum and jejunum. B1 no chemo. * Anal cancer is squamous cell. * Negative colonoscopy at age 50. Rectal cancer on the other hand needs surgery and radiation. maybe chemotherapy depending on the stage of rectal cancer. Tubular is a histologic description. submucosa. Early anal cancers can be cured without surgery using chemotherapy and radiation instead. Then you would have to do a complete colonoscopy to clear colon. goes locally to lymph nodes then liver (not lungs or bones without going through liver first as a rule). C2 means full thickness with lymph nodes. ulcer disease. patient needs to go to surgery and have cancer removed with clean margins on each side and management of blood vessels. * Malignancy found on colonoscopy. * Cause of upper GI bleeds include esophageal varicose veins. Patients can tolerate these medications so useful for outpatient chemotherapy from 6 months to a year. melena (acid degrading blood. * If polyp is hyperplastic. A couple decades from now colon cancer may be deeper down the list instead of the third most common cancer in men and women. Duke B is controversial. * Duke D cancer is distant metastasis. * Other causes of dark or black stool are patients taking iron supplements and patients taking oral bismuth. HPV is the precursor to cervical cancer in women. * Virtual colonoscopy is a CT scan of the colon and is not standard of practice currently. * The better we get with colon cancer screening and polyp removal. patient has to come back to make sure no new polyps have grown back.Study Notes – Internal Medicine James Lamberg 28Jul2010 * Around 30% of Americans have adenomatous polyps after the age of 50. Mallory-Weiss tears. * Test of choice is upper GI endoscopy. or duodenal bulb. * Sigmoidoscopy with barium enema is less expensive and less likely to have a complication such as a perforation. Villous histology has a higher potential to become malignant. get blood bank ready if needed. HPV warts (condyloma accuminata) are precursors to anal cancer. you have to remove the cancer first before chemo. anastomosis of colon ends together.61 - . Squamous mucosa does respond to chemotherapy and radiation. stomach. Chemo should be given for Duke C as the cancer is localized but not systemic. The veins are collateral circulation that become engorged. B2 means full thickness but not through. * Chemotherapy is never curative for colon cancer. They will say if it is tubular histology or villous histology. patient can wait 10 years until next colonoscopy. then think about whether the patient needs chemotherapy or not. pathologist will give you additional information. * Radiation is useful for advanced rectal cancers. hemorrhoids too. * If polyp is adenoma. such as alcoholic liver disease or hepatitis C induced cirrhosis. * 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. * If adenoma polyp is found. Example would be a general surgeon or non-gastroenterologist doing a sigmoidoscopy and doing a biopsy of a polyp instead of polypectomy. B2 maybe. send blood for type and cross. * Duke B cancer goes into layers of the bowel wall but not through it. past mucosal layer. * When do we give chemo? Duke A patient is cured so not needed. Colonoscopy involves IV sedation so there is risk there too. Upper GI barium series has no role in the management of active upper GI DO NOT DISTRIBUTE . it is not premalignant. the less likely Americans are to die from colon cancer. * Varicose veins is due to portal hypertension from liver disease. patient cured almost for sure with surgical resection. * Duke C cancer does not go through full thickness but has lymph nodes.

the aorta and internal iliacs. * A clue that rectal blood is from an upper GI bleed is an increased BUN/Cr ratio. * Medical therapy is not as useful for controlling GI bleeding. which is why the nuclear scan is done first. In elderly. but very few things bleed in the small intestine. just formed brown stool. * A red blood cell scan in the abdomen should show you the vasculature normally. If the patient continues to bleed. so you see the bleeding diverticuli then go higher and see no blood. Pancreatitis * Acute pancreatitis presents as abdominal pain. given as IV bolus then hourly infusion typically for three days if the patient has esophageal variceal bleeding. It is done if the nuclear scan cannot be done or the nuclear scan is not diagnostic. type and cross blood. the surgeon is stuck and has to do a sub-total colectomy taking out the whole colon down to the rectum. Also nuclear scan is less invasive and can be repeated over several hours. so BUN raises out of proportion to creatinine. Alcohol is a direct toxin to the pancreas DO NOT DISTRIBUTE . you should suspect Meckel diverticulum. called Meckel scan. or during the prep the bleeding could have stopped. IV PPIs might help.Study Notes – Internal Medicine James Lamberg 28Jul2010 bleeding. Bleeding events may be episodic. can be done laparoscopically. if the cells are leaking out somewhere they will accumulate in that area. * If major bleeding. sometimes diffuse tenderness. painless bleeding. You would see gastric cells light-up in the small bowel. next step is stabilization. AVMs usually found in ascending right side of colon. angiodysplasia was previous name). It requires more active bleeding than a nuclear scan. Say the patient his diverticuli along the whole colon and you see lots of blood on colonoscopy. A local external exam or short-scope anoscopy can show hemorrhoids or fissures that are bleeding. Octreotide is 8 peptides. so if you see them do not assume that was the cause. we generally send the patient to surgery.62 - . You can see anorectal bleeding or on occasion see diverticular bleeding. then the bleeding scan can help localize the problem area. * Management of choice is endoscopic hemostasis. * 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. * Lower GI bleeding is defined as distal to the ligament of Treitz. * During angiography. * Say you do flexible sigmoidoscopy and it is non-diagnostic. Hopefully the bleeding scan pinpoints the area for localized resection. An angiogram requires active bleeding to be positive. You do colonoscopy and it is non-diagnostic. usually epigastric with/without radiation to back. * If the bleeding scan is non-diagnostic and the patient continues to bleed from diverticular disease. * Exception is children or young adults with negative colon testing and painless blood emanating through ileocecal valve. 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). AVMs more commonly seen in patients with aortic stenosis (controversial idea). next most common is diverticulosis then arteriovenous malformations (AVMs. * Most common cause of mild (small amount) painless rectal bleeding is hemorrhoids or fissures. Octreotide is a synthetic analog of somatostatin and reduces portal pressures. Exception is variceal bleeding. Next step if the patient is actively bleeding is a bleeding scan where nuclear label is mixed with the patient’s red blood cells. give fluid. which would imply right colon. * Diagnosis of Meckel diverticulum done with a bleeding scan that labels gastric mucosa. associated with nausea and vomiting. they require a resection. Sigmoidoscopy can be done immediately. 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. but might not be diagnostic. * Hematochezia or maroon stool (not BRBPR. Many people have diverticuli that do not bleed. in between) is likely colonic bleeding. * If esophageal varices. * The colonoscopy can show the location of the bleed. Endoscopy allows you to make the immediate diagnosis and even treat the source. Start large bore IV(s). * Most diverticular bleeds stop spontaneously and do not require surgery. You should not see a blush or collection on the right side. injected back into the patient. no melena. typicaly AVM. Gastric mucosa arrives in the diverticulum and acid production can cause ulceration of the diverticulum causing bleeding. Exam shows tenderness in mid-epigastric region. Blood is not absorbed in the colon so BUN/Cr would not increased with a straight colonic bleed. 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. endoscopist can inject a sclerosing agent or place rubber bands over veins (banding). * Diverticulosis usually found in sigmoid. * Medical management for esophageal varices specifically is octreotide. If the patient stops bleeding from diverticular disease and then restarts. then looking for the bleeding source. physician can inject the blood vessel locally with the angiogram catheter or maybe put a coil in to stop the bleeding. * Angiography is rarely used. * Nearly all cases of acute pancreatitis are caused by alcohol or gallstones. Treatment is resection.

O2. patient can get an operation called a Puestow procedure. and Dubin-Johnson syndrome are problems with indirect DO NOT DISTRIBUTE . * Common bile duct obstruction with cholangitis should be treated via ERCP stone extraction. which is problematic because in general they are alcohol addicts and you run the risk of making them narcotic addicts from iatrogenic prescribing. * Gallstone pancreatitis is usually associated with a history of biliary colic (crampy RUQ pain after meals). 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). * Blood test abnormalities are described in Ranson prognostic criteria. * Mnemonic (admission): GA LAW. All the proteolytic enzymes cannot leave the pancreas so you get autodigestion of the pancreas by the enzymes. * Treatment for cholangitis should also include antibiotics. * Treatment of gallstone pancreatitis that does not resolve on its own is endoscopic retrograde cholangiopancreatography (ERCP) with stone removal. Bilirubin may climb to 5 or 6 here. meets with splenic vein into the portal vein and through liver. Then you know most of the bilirubin is unconjugated. hemolysis). so insulin dependent diabetes but not Type I. Bile and even pus may pour out and patient gets better. If the pain is very severe. Pseudocyst can cause obstruction.63 - . Chronic pancreatitis is usually associated with alcohol use. Heme part of RBCs is broken down to biliverdin then to bilirubin. Other important symptom of chronic pancreatitis is chronic abdominal pain. correction of hypochloremic hypokalemic metabolic acidosis. * The SMA feeds the small intestine and the SMV. * Inflamed swollen boggy pancreas is called a phlegmon (spreading diffuse inflammatory process with formation of suppurative/purulent exudate or pus). AST. it is due to chronic pancreatitis. and hemosiderin producing a golden-brown color. * Mnemonic (48 hours): C HOBBS. That bilirubin is the one that ends up in your bloodstream making you yellow or into kidneys making urine tea or cola colored. thus high unconjugated bilirubin will not darken the urine.0 and indirect is 3. biliverdin producing a green color. fever. calcium. Bilirubin is also metabolized here. do a CT scan to rule out pancreatic abscess. * Gilbert (pronounced jheel-BAYR). Initial testing can include CT scan.Study Notes – Internal Medicine James Lamberg 28Jul2010 causing inflammation. fistulization into the lung causing pleural effusion (send fluid for amylase). * Chronic pancreatitis can present with exocrine insufficiency as maldigestion and we treat them with pancreatic enzyme replacement. now pancreatic enzymes drain right into the jejunum preventing irritation of the pancreas from trapped enzymes. For ICU patients. base deficit. Crigler-Najjar. glucose. WBC count. * The colors of a bruise are caused by the phagocytosis and sequential degradation of hemoglobin to biliverdin to bilirubin to hemosiderin. It is also an important detoxification organ and nutrition absorption organ. hematocrit. Bilirubin bound to albumin travels via portal system to liver hepatocytes where it is conjugated to glucuronic acid giving bilirubin glucuronide. * Say total bilirubin is 5. Mortality 100% if score 7 or 8. age. * Gallstone pancreatitis never leads to chronic pancreatitis because patient either gets better or goes for stone extraction with ERCP. BUN. A stone would need to block either the common bile duct and/or the pancreatic duct (choledocholithiasis). IV hydration. Indirect is unconjugated bilirubin. * Initial labs should include amylase and lipase. bilirubin producing a yellow color. * If patient is not getting better after a few days of NPO and IV fluids for pancreatitis. Say total bilirubin is 10 and indirect is 9. * Total bilirubin is direct + indirect bilirubin. after taking in intestinal nutrients. * Puestow procedure (longitudinal pancreaticojejunostomy) can be useful to prevent narcotic addition or to help a patient who is already addicted to prescription narcotics. * Treatment is to put the pancreas at rest. and jaundice. they need surgical debridement of the abscess or even radiology-guided needle aspiration. Albumin bound bilirubin coming out of spleen is not water soluble and is not urinated. Direct is conjugated bilirubin. NPO because food stimulates the pancreas. * RBCs last about 120 days and get trapped in spleen in the reticuloendothelial system as they break down. NG tube if need to decompress the stomach (if vomiting). Liver Disease * Liver is an important synthetic site for many compounds such as albumin and coagulation factors. and localized pancreatic abscess occurring in a few days. sequestration of fluid > 6L. you may need to do follow-up CT scans and drain any new cysts/abscesses. Calcium becomes deposited through duct system of the pancreas and can be seen on plain film indicating chronic calcifying pancreatitis. Cholangitis is classically with Charcot triad of RUQ pain. pain. exocrine pancreatic insufficiency. with hemoglobin itself producing a red-blue color. Procedure filets open the pancreas then sew a loop of jejunum into the bottom of the pancreas. Severe pancreatitis is likely if score 3+. lipase is more specific. LDH. then you know this is not a liver problem (spleen problem.8. If pancreatic abscess. which was originally developed just for alcoholic pancreatitis. They can present with endocrine insufficiency as diabetes with insulin dependence from beta cell destruction.

Dubin-Johnson prognosis is much better with most patients living normal lives. liver disease. can be transmitted via seafood. Test of choice is ERCP with dye injection to visualize biliary tree. * Hepatitis A does not become chronic so patients cannot get cirrhotic or get a hepatoma. separate process from bilirubin. high copper in 24h urine. Tell patient about the syndrome to help prevent medical testing in the future (ultrasounds. Incubation period is a couple of weeks. there will be a high indirect bilirubin. liver transplantation if needed and for cure. post-mortem liver may look black or dark-pink. fatigue. * PBC treatments do not work very well and patients will get cirrhosis at some point. liver transplant. Past major cases involved strawberries and green onions. so biopsy not need but a picture of the ducts is needed. anorexia.64 - . fevers. There is likely a family history of liver disease. get before you travel to endemic areas or get because universally recommended. Viral Hepatitis * Hepatitis A can be asymptomatic and IgM (active infection) positive. Organs include eye (Kayser-Fleischer ring). would lead to jaundice and pruritus. Eventually patient will get cirrhosis from this. almost all indirect) and worry about liver problems. no signs of hemolysis. As this disease progresses the patient will need liver transplantation. * Hemochromatosis. Patient presents with pruritus as the earliest symptom. which is copper chelation from bloodstream. showing beads on a string pattern. malaise. seeing damage to microscopic bile ducts. Gene for alpha1-antitrypsin is located in liver so new liver corrects the problem. Gilbert syndrome is a problem with the uptake and conjugation due to deficiency of glucuronyltransferase. * Hepatitis A vaccine exists. Labs show high serum copper. Organs are liver. Then the patient becomes jaundiced (elevated conjugated bilirubin). Past exposure can be seen with IgG antibody.g. Test to do is hepatitis A IgM. bilirubin. Classic is stricturing and narrowing of the biliary tree. ALP is the first blood test to become elevated. This is sclerosing of the larger macroscopic bile ducts. * Treatment of Wilson disease is penicillamine. Family history of liver disease. Liver transplantation is curative. Most cases are mild. Chief problem with Gilbert syndrome is you see the bilirubin (2-4. * 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. 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). * Younger man presenting with pruritus. and alpha1-antitrypsin deficiency are hereditary liver disease. Bile salts derive from cholesterol synthesis and are needed for fat digestion. With a mechanical blockage of the bile duct we have conjugated bilirubin backing up into the bloodstream making you jaundice. Other drugs include zinc and triene. increased ALP.Study Notes – Internal Medicine James Lamberg 28Jul2010 bilirubin. Patient is asymptomatic but may get mild jaundice (e. Hepatitis A is fecal oral. Bile salts are also conjugated and hydroxylated. Do not confuse PSC with PBC. electrolytes. * Autoimmune disease against the microscopic bile ductules is primary biliary cirrhosis (PBC). DO NOT DISTRIBUTE . heart (cardiomyopathy). Diagnosis is via liver biopsy. Suspect in patients who have emphysema and are non-smokers or if patient has relatives with precocious emphysema. If patient has progressed to cirrhosis and portal hypertension. The only one you will probably see in clinical practice is Gilbert syndrome. increased bilirubin. Reticulocyte count is normal. biopsies). All can progress to cirrhosis and end stage liver disease. Autoimmune marker is anti-mitochondrial antibody is suggestive. scleral icterus) at times of stress. Crigler-Najjar presents at birth and requires major medical and surgical therapy (phototherapy 12h/day. Trypsin originates in the liver and is inactivated by alph1-antitrypsin. low grade fevers. RUQ tenderness. PSC is associated with ulcerative colitis. Antibody that is positive but not too useful in diagnosis is ANCA. * Hemochromatosis is hyper-absorption of iron in the intestine and deposits of iron in various organs. skin (“bronze diabetes”). pancreas. Management at that point is liver transplantation. and bile salts. This is almost always seen in middle-aged women (40s-60s). Example scenario would be a nursing home or kindergarten outbreak where kids and teachers get jaundice. They all have another organ involvement to suggest them. * Blockage of the common bile duct. CNS (choreoathetosis. they will need liver transplantation which is curative. dementia). transfusions). but know penicillamine. * Alpha1-antitrypsin deficiency leads to unopposed action of trypsin which is a proteolytic enzyme. Bile contains water. low levels of ceruloplasmin (copper carrying protein). * Treatment of alpha1-antitrypsin is limited. Disease is primary sclerosing cholangitis (PSC). * Wilson disease is a problem with excess copper deposition in the liver due to poor excretion from GI tract in bile. Blood test is alpha1-antitrypsin level. Diagnosis confirmed by liver biopsy staining for copper (Timm silver stain). * Crigler-Najjar and Dubin-Johnson syndrome are very rare and are problems secreting bilirubin from the hepatocyte. The bile salts in the bile give you the pruritus. Ultimate diagnosis rests in liver biopsy. Diagnosis is via liver biopsy and stains for iron on that biopsy (Prussian blue). Typical symptoms of hepatitis are jaundice. Wilson disease. such as intrahepatic stricturing or stone. Organs affected are liver and lung.

TSH is up and TRH is up. * Medical treatment for hepatitis B includes antiviral drugs lamivudine. * Treatment of prolactinomas is bromocriptine. Anyone exposed to blood or sexual contact should be vaccinated so health care workers. With primary hypothyroidism. prostitutes. and entecavir. specifically bitemporal hemianopsia. TRH activates TSH release and that activates T3/T4 release from thyroid. do not jump to adenoma as the cause. fevers. TSH. Thus there is minimal pressure phenomenon. * If prolactin level is elevated. secreting hormones (ACTH. MD -------------------------------------------------------------------------------------------------------------------------------------------Pituitary Disease: Hyperpituitarism * Pituitary gland is on the sella turcica surrounded by the sphenoid bone and around that area is the optic chiasm. TRH is not tested for because it is expensive and has to be sent out. or chronic hepatitis B that has become newly activated. True hepatitis infection in the past would be HBsAb and HBcAb. * Pituitary is divided into posterior and adenohypophysis. eventually cirrhosis and hepatoma (hepatocellular carcinoma). It is fecal-oral and not common in the United States. headaches. They usually present with visual field cuts. Test is PCR for hepatitis C where we can measure quantitatively how much hepatitis C there is. * 32yo woman comes to your office because she has noticed a milk-like discharge from her breast for the past four weeks. Transaminases increased are SGOT (AST) and SGPT (ALT) from 50 up to 200 max. Stages of control are hypothalamus. Getting the vaccine only would be HBsAb without HBcAb (surface without core). Every case of hepatitis C becomes chronic. * Hepatitis D is a co-infection with hepatitis B.65 - . jaundice. tenofovir. * Hepatitis B transmitted via blood or sexual contact. If minimal activity then might not need treatment. She is on no dopamine depleting medications and has a normal TSH and T4. Interferon can be used as well. Treatment used for moderate hepatitis C prior to cirrhosis progression. which is a dopamine activator and thus a prolactin inhibitor. If progressed to cirrhosis then it is too late to treat. hepatitis B surface antibody (HBsAb) and hepatitis B core antibody (HBcAb). pre-1989 via transfusion or needlestick injury or dialysis worker or IV drug abuser.hemianopsia. the prolactinoma is usually a microadenoma. IV drug abusers. * There is a hepatitis B vaccine. When dopamine is inhibited or if autonomous adenoma will you get prolactinemia. Charles Faselis. you are labeled as chronic hepatitis B.Study Notes – Internal Medicine James Lamberg 28Jul2010 * Hepatitis B patients are generally symptomatic. Hepatitis B can become chronic and thus develop cirrhosis and hepatoma (hepatocellular carcinoma). Usually adenohypophysis secretes hormones that affect organs in the periphery. fatigue. it usually does not present acutely. * Hepatitis E has a high mortality in pregnant women. give alpha-interferon subcutaneously and ribavirin. Posterior pituitary secrets oxytocin and ADH. So pituitary disease commonly affects visual field. think prolactinoma because these are the most common active pituitary tumors. DO NOT DISTRIBUTE . Prolactin is under continuous inhibition from dopamine. TRH at high doses seems to be an activator of prolactin. and end organs. It is seen in epidemics. Check for TSH. a major risk for health care workers. telbivudine. They secrete autonomous prolactin. and pressure phenomenon. * Hepatitis C transmitted via blood usually. Decreasing production of prolactin from a prolactinoma would shrink the size of the tumor. They rarely present with gynecomastia or galactorrhea. * In women. pituitary. No need to treat everyone. Look for other causes like dopamine inhibitors like haloperidol (depletes dopamine) and primary hypothyroidism. Suspect hepatitis D in severe cases of hepatitis B. Hopefully you become immune if you body creates the appropriate antibodies. which are produced by the hypothalamus and stored in the pituitary. which has low T3 and low T4. Examination reveals galactorrhea but is otherwise normal (no visual field cuts or amenorrhea). do liver biopsy to assess activity. -------------------------------------------------------------------------------------------------------------------------------------------Kaplan Videos (2001) – Endocrinology with Dr. * With galactorrhea. * Hepatitis C presents with chronic fatigue and chronic transaminase elevation. There is not much we can do about hepatitis D. typically seen in patients with a high titer of hepatitis B like patients who continually use IV drugs. There is no vaccine for hepatitis C. alpha-interferon with ribavirin. 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). etc. They usually presents with amenorrhea and galactorrhea +/. In a normal individual hormone. RUQ pain. do an MRI of the pituitary to look for the lesion. * 32yo woman comes in with galactorrhea. Active infection serology is hepatitis B surface antigen positive (HBsAg). * In men. the prolactinoma is usually a macroadenoma. etc) and is affected directly by other hormones in the hypothalamus. What is the next test to order? Answer is prolactin level. If after six month of HBsAg positive without HBsAb. * Medical treatment for hepatitis C is pretty good. Also others like adefovir. * With galactorrhea presentation.

* In rare scenarios. Somatostatin is a statin of somatic activity. administer appropriate hormones.66 - . done by a glucose tolerance test. normal response is decrease in growth hormone. It may occur because the patient is missing ADH. and those are FSH. high-dose corticosteroids. Patients usually have a pre-existing pituitary adenoma that was not treated well or not treated at all. Then do the MRI looking for the tumor in the pituitary. This can occur even 5 years after pregnancy. thus cannot be easily visualized on CT or MRI. called central diabetes insipidus (CDI). high GH. which has an effect on tissue and bone causing it to grow. You can also check the levels of FSH and LH in the blood. nuchal rigidity. * DI patients complain of polyuria and polydipsia. Appropriate response is no insulin release and elevated counter-regulatory hormones. Then TSH is lost. Pituitary Disease: Hypopituitarism * Hypopituitarism is loss of pituitary hormones over time. and trauma to the head. Lastly you lose the most important. which shrinks the size of the tumor in acromegaly for unknown reasons. * Treatment for acromegaly is octreotide (somatostatin). * 80% of acromegaly patients have elevated glucose and about 30% of them have diabetes mellitus. LH. If glucose is high. The adenoma increases in size and the patient bleeds into the adenoma then virtually blows out their pituitary. antidiuretic hormone (ADH). If after glucose load. and growth hormone. * Patients with empty sella syndrome usually have normal endocrine function. * Screening test for hypopituitarism is the insulin-tolerance test. but the ADH cannot work because the DO NOT DISTRIBUTE . which would always be elevated in acromegaly patients. This is needed to concentrate your urine. * We could also measure ILGF levels. * Nephrogenic diabetes insipidus (NDI) occurs when ADH is in high levels. prolactinomas occur in older women. In this case. and organs grow such as the heart which leads to congestive heart failure and is the most common cause of death. evaluate electrolytes. * Before considering a MRI of the pituitary (80-90% of cases) in acromegaly. shoe size. granulomas. Screening test for acromegaly is to give the patient glucose then measure growth hormone after an hour. it would be stroke syndromes. The first hormones to be lost are the ones you need the least. Surgery and radiotherapy are also options. So you expect high glucagon. tongue grows. You measure growth hormone an hour later and expect it to be elevated. you are not worried about pregnancy so you can watch the patient and not treat if there is no pressure phenomenon. growth hormone is elevated. namely stroke syndromes. You can check the cortisol level at the same time to see if ACTH is missing too. granulomas in the brain. probably hypopituitarism. The meninges come into the sella and push out the pituitary. * In children. ring size. high cortisol. this is an inappropriate response and we say the patient likely has acromegaly due to autonomous hormone release. jaw grows.Study Notes – Internal Medicine James Lamberg 28Jul2010 * Treatment of prolactinomas that are macroadenomas (usually men) may need surgery or radiotherapy. Acromegaly is due to hypersecretion of growth hormone. History is patient with pituitary adenoma comes in with stupor. * Pituitary apoplexy is a medical emergency. the patient is missing the diaphragmatic surfaces holding the pituitary in. ILGF are somatomedins. * Treatment of Sheehan syndrome is to replace hormones they have lost. larger feet. Next treatment option is bromocriptine. somatomedins). * Treatment of pituitary apoplexy is medical stabilization. glucagon. Growth hormone mainly works through the liver by secreting insulin-like growth factor (ILGF. CDI can occur with any space occupying lesion or anything affecting the central nervous system. If it looks like Sheehan syndrome. You can live without these. you have to document that the patient has autonomous hypersecretion of growth factor. and cortisol. normal response is increased insulin and decreased counter-regulatory hormones. Insulin puts glucose into cells and lowers blood glucose. So the pituitary is pushed off to the side and squished between the meninges. cancers. Counter-regulatory hormones keeps glucose levels high in the blood. You cannot have empty sella syndrome with normal endocrine function. Pituitary Disease: Posterior Pituitary * Diabetes insipidus (DI) occurs when patients are missing the major water-retaining hormone in their body. The most common in children is a craniopharyngioma. These patients had no endocrine issue but got a CT or MRI for another procedure and were found to have an empty sella. * Acromegaly symptoms are enlarged head. and headaches. In empty sella syndrome. Give patient 5U of insulin to cause hypoglycemia. ACTH which affects the adrenals. tumors in the brain. or mediators of somatic activity. * Sheehan syndrome usually occurs after a prolonged and labored pregnancy. which is a bit more important. In adults. The first sign of Sheehan syndrome is the inability to lactate. vomiting. do the insulin tolerance test to make sure it is not hypopituitarism. * Glucose causes the release of insulin and counter-regulatory hormones like growth hormone. You do not just measure GH because it changes throughout the day so you have to provoke it. any space occupying lesion can cause hypopituitarism. If GH is not high an hour after 5U insulin given. neurosurgical consult for transsphenoidal decompression of the tumor. else you lose free water. * Acromegaly with pituitary adenoma is caused by a macroadenoma 75% of the time.

serum Na+ is increasing. At the same time. you would give T3 hormone. and finally decreases urine output. These patients hold on to too much free water. trauma. * In severe hyponatremia. tuberculosis.67 - . * Insipid means devoid of characteristic. nearly all of it is bound to albumin. To see how the thyroid is really working. which increases proximal sodium and water reabsorption. T4. not the total because you only care about free T4. Thyroid Function Testing * Thyroid gland produces T4 as the main secretory product.Study Notes – Internal Medicine James Lamberg 28Jul2010 receptors in the kidney do not function. Desmopressin is like ADH but only different by one amino acid. so as they are getting more dehydrated they will keep putting out dilute urine. and T4/T3 from thyroid. * Psychogenic polydipsia is characterized by large intakes of water and large outputs of urine. 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. * Test for DI is the water deprivation test. * SIADH can occur with lung processes like abscess. and has the feedback effect to TSH and TRH. so they can take in 20L and put out 20L. * 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. you want free T3 and free T4. Because T3 is more potent. you cannot differentiate CDI from NDI. If the patient has no ADH (CDI). These patients do not wake up in the middle of the night to go to the bathroom. This is why we need to objectively assess the thyroid by looking at thyroid hormones. The causes of NDI are lithium and demeclocycline. Forget about the T4 and forget about the T3. so does nothing to TSH or TRH for feedback nor does it have metabolic effects. so diabetes insipidus has dilute urine. COPD. It is when they lose access to water that they get very dehydrated. pituitary (TSH). so you give the patient vasopressin (ADH). At this point. Sometimes the sodium is so low we have to treat the SIADH.1% of the total. which increases urinary excretion. but they are putting out dilute urine (Uosm low/not changing). This is called thyroid binding globulin and it is an inactive form. which dilutes the sodium and causes hyponatremia. strokes. The mechanism for thiazide diuretics is to decrease distal tubular sodium reabsorption. so they are very good tests. which decreases distal delivery of sodium and water. * Patients with DI usually have access to water. Treatment of choice is water restriction. * When your thyroid puts out T3 + T4. * If the TSH is normal. The free T4 is less than 0. in general that patient is euthyroid. This disease runs in families. The thyroid produces mostly T4. this can only be NDI since the kidney receptors are not responding to ADH. * T3 is a more potent hormone with a better effect. Do not replace too quickly due to risk of central pontine myelinolysis. the patient does not make urine to conserve free water. * SIADH can occur with medications like vinblastine and vincristine. however you do not have the pressor effects of ADH. In a normal individual will get dehydrated and Posm will increase. A patient with DI cannot do this. then SIADH usually resolves. * Treatment for NDI is hydrochlorothiazide or amiloride. you will start to see a normalization of Uosm (Uosm increasing and concentrating). Normal is increased Posm and increased Uosm (urine concentrates). * Do not assume enlargement or nodules of the thyroid mean hyperthyroidism. * Treatment for CDI is to give vasopressin (ADH) or give intranasal desmopressin. * Syndrome of inappropriate ADH (SIADH) secretion is when patients produce small amounts of concentrated urine. If you give ADH and there is no change in Uosm. Correcting hypernatremia too quickly with free water can result in cerebral edema and seizures. it has a stronger feedback. Treatment could also include drugs that cause NDI like lithium and demeclocycline. it is metabolically active. * Thyroid levels of control are hypothalamic function (TRH). but also think about psychogenic polydipsia. and TSH (indirect measurement). demeclocycline is probably preferred due to less side effects and less drug-drug interactions. hypertonic saline can be used. Posm will increase. which decreases extracellular volume. The current TSH testing can diagnose hypothyroidism or hyperthyroidism with a 95% confidence interval. T3. The diuretics get rid of sodium and help retain water. Water deprivation test will show almost normal response. where plasma osmolality is plotted against urine osmolality. * Free T4 use to be a difficult test. granulomas. This sounds like a paradox because the patient is getting rid of lots of urine. * Treatment of SIADH is to treat the primary disease. When these patients drink lots of water the wash out the medulla of the kidney and lose concentrating capabilities. * Patients presenting with polyuria and polydipsia either have diabetes mellitus (check serum and urine glucose) then think about DI. To suppress TRH and TSH. but the aim is to retain water. These drugs can make the ADH receptors in the kidney unresponsive to ADH. so people measured total T4 then got RT3U (resin T3 uptake) to indirectly DO NOT DISTRIBUTE . infections. * SIADH can occur with CNS processes like tumors.

then give thyroid medication (synthroid or any other T4 form). it is an indirect measure of T4. this test is not done anymore so look for a free T4 test. RAI-uptake scan high. The cause is an immune process. elevated total T4. Total T3/T4 would be down in this patient but it is not hypothyroid. Example is Graves disease. palpitations. LH. but you definitely DO NOT DISTRIBUTE . Radioactive iodine is given to the patient. or steroids. * Proptosis and exophthalmos commonly gets worse when you treat Graves disease. Propranolol can cause small for dates. but TSH came back normal. * A patient is intubated in the ICU and the patient’s FT4 was high or low. they have increased proteins so total T4 will increase. We can also use propranolol. Radioactive iodine has not been shown to cause cancer. free T4 elevated. This patient should not be treated with antithyroid medication. So we can only use these at low doses. * Primary hyperthyroidism: TSH low. So be careful when you see a total T4 or total T3 instead of free T4 or free T3. * Since 99. * Pregnancy or protein-increasing medication: TSH normal. free T4 elevated. Resin T3 uptake does not measure T3. Give them a little bit of PTU and propranolol to cool down the thyroid. * If agranulocytosis occurs with PTU then you cannot give the patient methimazole. and elevated RAI-uptake if you felt you needed it. increased FT4. Normal is 1040% uptake just as a note. Anything under this would be hypothyroidism. diarrhea. * Exogenous thyroid medication use (e. * Thyroiditis: TSH low. so you have to follow this patient every six months to check thyroid hormones. When they become hypothyroid. The thyroid enlargement is diffuse and is the only time in thyroid disease where you get proptosis and exophthalmos. Example is hypopituitarism. free T3 elevated. RAI-uptake scan is low. weight loss attempt): TSH low. free T3 normal. Thyroid hormone is being spilled into the periphery due to destroyed thyroid cells but uptake is low because thyroid is injured. menstrual irregularities. they likely have a lot of other comorbid conditions. Example patient with nephrotic syndrome or cirrhosis. or orbit radiation. It is reversible agranulocytosis as long as you catch it. * Secondary hypothyroidism: TSH low. * With fluctuations in protein the body will keep the free T3 and free T4 stable. free T3 elevated. If patient is on this medication and calls you saying they feel horrible and are running a high fever. Tell them to stop the medication and have their white cells checked. * In pregnant patient with Graves disease the only anti-thyroid medication we can use is PTU. * Anti-microsomal antibodies sometimes associated with Hashimoto disease. * Management in the acute phase is to relieve symptoms and reduce peripheral thyroid hormone. free T4 low. RAIuptake scan low or normal. atenolol) until patient is out of acute phase meaning they feel better and become euthyroid. Likely to have abnormal growth hormone. Is this patient hyperthyroid? No. tachycardia. Example is subacute thyroiditis. * Thyroid globulin immunoglobulin sometimes associated with Graves disease. Free T4 in this patient would be normal and TSH would be normal. * Graves laboratory findings would be low TSH. Again.68 - . bruit over thyroid. * Complication of PTU and methimazole is agranulocytosis. RAI-uptake scan normal. Example would be pregnant patient or patient taking estrogen. Symptomatic relief includes beta-blocker therapy (propranolol. Within months or years the patient will become hypothyroid. Free T4 and TSH would be normal in this patient.g. repeat in 48h to see what the uptake is. and FSH because usually not just one pituitary hormone missing. Since this is an ICU patient. any changes in albumin and protein levels in the body will fluctuate the total T3 and total T4 levels. then scan the thyroid. Both of these cross the placenta and have side effects. antibodies that affect the TSH thyroid receptors. treatment is to wait. free T4 elevated. So they may need surgery. antibodies act like TSH to rev-up the thyroid. free T3 elevated. * Other Graves signs include dermopathy. sometimes swelling of the feet (pretibial myxedema). * Radioactive iodine uptake scan (RAI-uptake) is a way to directly measure function o the thyroid. Anti-thyroid medications are propylthiouracil (PTU) and methimazole to decrease thyroid hormone level. they will get agranulocytosis with that as well. RAI-uptake scan is low. Ophthalmopathy is treated separately as patient may not be able to close their eyes and may get eye ulcers.9% of thyroid hormones are bound to albumin. weight loss. wait 24h. Thyroid hormones use to be in weight reduction medication a few decades ago even in this country. Hyperthyroidism * Graves disease is the most common cause of hyperthyroidism. Someone thought this patient might have a thyroid problem. * Management after acute phase is definitive treatment with radioactive iodine to kill the thyroid. free T4 low. toxic nodular goiter.Study Notes – Internal Medicine James Lamberg 28Jul2010 measure free T4 index. tremor. then take the patient to surgery in the second trimester. total protein level is down. anything over this is hyperthyroidism. intolerance to heat. There is no need for endocrine management here. free T4 normal. This patient has sick euthyroid syndrome.

maybe one. so giving the patient iodide will down-regulate the production of T3/T4. It would rather grab onto iodide. a type of dementia can form. * Symptoms of hypothyroidism include weight gain. you want to give this slowly in the elderly patient who may have coronary heart disease. * Chronic low-grade inflammation of the thyroid will eventually lead to fibrosis and destruction. * Treatment is propranolol even if they have hypotension. * Treatment for thyroid storm also includes fluids. These patients will usually present with hypothyroid symptoms as the thyroid has been destroyed. This causes spilling of T4 and T3. * Can have antimicrosomal antibodies. cooling blankets. and steroids because of hydrocortisone dysregulation. are hypothermic and are sometimes found out in the cold (cold or infection precipitated the untreated hypothyroidism). * Thyroid storm usually in patients with Graves disease and precipitated by a condition such as infection or surgery.69 - . DO NOT DISTRIBUTE . ESR will be elevated always. * Presentation occurs mostly in elderly patients and they have mainly cardiac manifestation such as atrial fibrillation. * Toxic nodular goiter is more common in adults and older patients. The thyroid eventually dies out and the patient becomes hypothyroid. replace thyroid hormone. start at 25mcg/day then go to 50mcg/day then consider going up if needed. Inflammatory process can be acute where there is intense inflammation of the thyroid. cholesterol increases due to lack of metabolic hormones. so these patients usually present with hyperthyroid symptoms. This is high output cardiac failure. * Post-partum thyroiditis is subacute thyroiditis after delivery. * This is subacute thyroiditis. These patients have altered mental status. Thyroiditis * Thyroiditis is an inflammatory condition of the thyroid gland and is relatively common. * A normal adult mainstay does is 100mcg/day. hypotension. conservative management. Order the RAIuptake test. low FT3. maybe many. * Treatment is the same as all hypothyroidism. Elderly patient may develop chest pain and may even get a myocardial infarction. acute inflammatory markers will be elevated.Study Notes – Internal Medicine James Lamberg 28Jul2010 do not want to give it to a pregnant patient. a couple days later they will have more iodide so they can produce much more T3/T4. * This is Hashimoto thyroiditis. Exam shows decreased deep tendon reflexes specifically the relaxation phase. Also give fluids. * Lab profile is high TSH. * Toxic nodular goiter exam will not show a diffuse enlargement. and steroids (hydrocortisone). This is an immune process where there is production of antibodies and lymphocytes that cause chronic inflammation of the thyroid. Thyroid Storm * Thyroid storm definition is a hyperthyroid patient with delirium. * Hashimoto associated with other autoimmune diseases such as pernicious anemia. which will be low. * Treatment is thyroid hormone replacement usually in the form of T4. Palpation of the thyroid results in pain. tachycardia. * Elderly patient develops dementia. Hypothyroidism * Most common form of hypothyroidism is Hashimoto thyroiditis. dry skin. * Iodide buys you some time. Remember high doses of T4 given. Biopsy here will show lymphocytic infiltrate. these patients will become euthyroid. treated with propranolol. and all of a sudden developed high cholesterol. * Because subacute thyroiditis is an inflammatory process. cold intolerance. also called De Quervain thyroiditis or giant cell thyroiditis. For elderly patient. Since these are metabolic hormones. * Myxedema coma is a severe form of hypothyroidism. * Labs for subacute thyroiditis show low TSH with high FT4/FT3. * Treatment of myxedema coma is high dose of thyroid hormone. If you do not manage the thyroid storm patient. same process. Patient is a little puffy and edematous. low FT4. Non-toxic goiter means nothing is being produced from the goiter. PTU. T3. and iodide. * Both hyperthyroidism and hypothyroidism cause proximal muscle weakness. which looks like Graves disease. * Iatrogenic hypothyroidism is also common in this country because of how we treat Graves disease. course hair. warming blankets. Subacute thyroiditis is most likely due to a viral infection. * Treatment is pain medication such as NSAIDs. Toxic goiter means the thyroid goiter produces thyroid hormone. CHF. has constipation. fever. In all severe thyroid problems there is dysregulation of adrenal steroid production. starting the process again. We also give the patient a more potent hormone. This is a very dangerous dose but it is the only way to treat these patients. Iodide is the cornerstone of thyroid storm treatment. These patients usually had a non-toxic goiter prior. periorbital edema. You will find nodules. Thyroid will either output T3/T4 or grab iodide but not generally both. fibrosis and scaring of the thyroid. constipation. congestive heart failure. After a week or month. transient. like T4 at 300mcg. aspirin.

So you cannot tell from only an FNA. Phosphate will always be low. no treatment available. decreases calcium by reducing bone resorption. so you would need to know that the treatment for that is radiation therapy (XRT) only to the head and neck. parathyroid hormone (PTH) increases. * Patient usually comes to the office complaining of a thyroid lump or you find one on routine exam. surgery then T3 or high dose T4. * When talking about PTH affect. which also has pheochromocytoma and neuromas. * Protocol for thyroid nodule found is to get TSH to see if functioning. * Iodine scan is a way to monitor these cancers. 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). follow patient but no management needed now. 80% of cases DO NOT DISTRIBUTE . then do thyroid surgery because that is the only way you can tell if this is a cancer or just a benign tumor. * PTH also affects the kidney to reabsorb calcium and the intestine to absorb more calcium through vitamin D. Ca++ is not a sensitive index of parathyroid hormone. usually grows focally and metastases to the lymph nodes around the thyroid. thyroid scan showing cold nodule.70 - . If thyroid cancer found on pathology of FNA. You have to do the FNA. * Treatment of papillary cancer allows for 95% of patient to live 5 years. Mnemonic: PTH. releasing calcium. associated lymphadenopathy. occurs in older individuals. This prevents hypocalcemia to the point of tetany and death. 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. activating osteoclasts. Parathyroid Disease * As a patient’s calcium goes down. * You notice in the family that patients have had solitary medullary cancer (not multiple endocrine neoplasia). * When PTH activates the kidney it wastes phosphate (PO4-). * Follicular cancer of the thyroid occurs in older individuals and usually has hematogenous spread. the calcium may be high or normal but the phosphate will always be low. older age. Think that this is likely follicular cancer. We can use salmon calcitonin to decrease calcium levels in hypercalcemia. phosphate trashing hormone. associated with radiation to the head and neck area. * Risk factor for thyroid cancer if you find a lump is radiotherapy to the head and neck (presumed to have cancer until proven otherwise). is slow growing. so great prognosis. Also associated with MEN-III (MEN-IIb). look at PO4-. This is because you do not know where the patient started with calcium. do not order a scan of any kind or an ultrasound. If TSH low the patient has some form of hyperthyroidism so you treat as hyperthyroidism (toxic nodular goiter). Next step in management is fine needle aspiration. But. then do surgery. They may just say the patient had Hodgkin disease stage IA several years ago. * With high levels of PTH secretion. * Calcitonin tones down calcium. about 70-80% of all primary thyroid cancer cases. then you know the patient has a non-functioning thyroid nodule and thus a chance for cancer. * Hypercalcemia found on routine screening 50% of the time it is primary hyperparathyroidism. * Vitamin D increases calcium and increases phosphate. PTH stimulates osteoclasts to break down bone and release calcium into serum. which also has pheochromocytoma and parathyroid hyperplasia. does not metastasize but it grows focally. If FNA is benign. Hyperparathyroidism * Primary hyperparathyroidism is the most common cause of hypercalcemia and is the most common cause of benign or mild hypercalcemia. * If a scan is done and a warm or hot nodule is found. * Other risk factors for thyroid cancer are male gender.Study Notes – Internal Medicine James Lamberg 28Jul2010 Thyroid Cancer * Papillary cancer of the thyroid is the most common. It is associated with some familial forms. one form being solitary medullary cancer. * Always do a fine needle aspiration on a thyroid nodule. the nodule has to be non-active meaning no hyperthyroidism. 10yr survival 80-90%. calcitonin producing cells). If TSH normal. If follicular elements are found on FNA. * 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. recent growth of nodule. * Patient presents with some kind of thyroid cancer and metastatic disease to distal visceral organs. * Exception is follicular cells found on FNA. * Papillary cancer is benign. * There is an autonomous adenoma that is producing PTH. * Medullary cancer of the thyroid arises from the parafollicular cells (C cells. * Treatment of follicular cancer is the same as papillary cancer. Less than 5% of patient live more than a couple of years. the next step is not waiting. The difference between a benign follicular adenoma and follicular cancer is the architecture. they can look for metastatic disease. * Anaplastic cancer of the thyroid is deadly. * Medullary cancer also associated with MEN-II (MEN-IIa).

Ionized calcium is the part that affects neuromuscular irritability. abdominal pain. The other mechanism is through production of PTH-like molecule. polydipsia. * Fibrosa cystica (brown tumors) develops in the bone due to the constant osteoclast activation resulting in cyst formation. Patient has hypercalcemia with severe peptic ulcer disease and diarrhea.8. Squamous cell cancer does not metastasize much. and parathyroid tumors. Diffuse granulomas seem to activate vitamin D. pituitary tumors. * Older individual with mild asymptomatic hyperparathyroidism may be watched. such as multiple myeloma. DO NOT DISTRIBUTE .Study Notes – Internal Medicine James Lamberg 28Jul2010 there is a single adenoma.5. only give furosemide if evidence of overload. * With one gland hyperplasia. Do not write for IVF and furosemide at the same time here. * Familial hypocalciuric hypercalcemia is a benign disorder. but their ionized calcium would remain the same. then calcitonin (immediate action. So sarcoid patients develop hypervitaminosis D in the summertime or when they go to sunny areas. * Hypocalcemia prolongs the QT interval. Lab would be low phosphate. * A patient with nephrotic syndrome would have a lower total calcium. it is given because the mainstay of treatment is fluids and we do not want to cause fluid overload in an elderly patient. This is the cause of the hypercalcemia (and more phosphorus too). After surgery. PTH level would be elevated only in primary hyperparathyroidism. this may be due to a gastrin producing pancreatic tumor (Zollinger-Ellison) with parathyroid tumor. * Normal albumin is 4mg/dL.71 - . * Treatment is surgery for definitive treatment. putting one in the arm. * Furosemide and diuretics can be seen in hypercalcemia protocols because furosemide gets rid of calcium. it should be done in all patients with symptomatic hyperparathyroidism such as kidney stones. polyuria. * To distinguish in a hypercalcemia patients between primary hyperparathyroidism and hypercalcemia of malignancy. you have three glands that are not working well. Treatment here is IV calcium with ECG monitoring for QT abnormalities. These are breakdown of bone. * Hypercalcemia associated with cancer is usually severe. make sure to account for low albumin states. Treat hypercalcemia with fluids (normal saline) primarily. no need for medications or further testing. so majority is protein bound. So PTH-like substance may not be picked up by parathyroid hormone levels. Furosemide does not do much to the calcium level. * Sarcoidosis can cause hypercalcemia. In 15-20% of cases there is four gland hyperplasia or parathyroid cancer. It is a chronic granulomatous disease. which activates the osteoclast. so hypervitaminosis D. These patients hardly ever have symptoms. With vitamin D deficiency and in some stages of chronic renal failure the parathyroid hormone becomes ineffective.6. This would be a nursing home patient who is in bed most of the time. Hypercalcemia causes shortened QT. Hypercalcemia of Malignancy * Hypercalcemia of malignancy can occur through multiple metastases to bones. * Most of vitamin D is absorbed in the summertime due to sunlight activation. Treatment is just to monitor the patient. They will have an elevated calcium level and it is not likely cancer or hyperparathyroidism. * Four gland hyperplasia requires removing all four glands. Watch these patients closely in a telemetry unit and monitor calcium levels for a couple of days.2mg/dL) = 2 * 0. Hypocalcemia after surgery for primary hyperparathyroidism is due to calcium going to bone and nothing left to stabilize the calcium. Hypocalcemia * Whenever you see hypocalcemia. the other three glands shrink due to negative feedback with calcium. Treatment is usually not necessary. A patient who got exploratory surgery around the neck area could have had damage to parathyroid gland circulation. then watching the serum calcium go up and down. So patient goes from hypercalcemia to hypocalcemia. wears off after 48hrs) or bisphosphonates (long acting) like pamidronate. What is this patient’s real total calcium? Answer is (4mg/dL . For every drop in albumin by a single point there is a drop in calcium of 0. osteitis fibrosa cystica. Fluids is the cornerstone of treatment for hypercalcemia. When we measure calcium in serum we get total calcium and 40% of this is ionized. So 6. Severe hypercalcemia occurs with > 15mg/dL and is a medical emergency. hydrochlorothiazide retains calcium. If calcium is still high. this is called hungry bone syndrome. Example is squamous cell lung cancer or esophageal cancer. * With hypocalcemia. * Most blood assays only check for parathyroid hormone that is intrinsic.8 factor = +1. it grows focally. giving diuretics if calcium is high or if kidney stones occur uncommon.5 + 1. think about hypoparathyroidism.1 total calcium. * Hypercalcemia of immobilization is also benign. so that is a case when you could give calcitonin at the same time as a bisphosphonate.6 = 8. * Primary hyperparathyroidism associated with MEN-I (the 3 Ps): pancreatic tumors. On the other hand. Say nephrotic patient is 2mg/dL albumin and total calcium level is 6. * Mild hypercalcemia would be bone pain. you order PTH level. where granulomas occur mainly in the lung but can occur anywhere.

but they do have diabetes. You do not have to treat the patient right away. * A Type I diabetic who presents at your office has not had the disease for very long. so these patients can break down lipids as their main form of energy which produces ketone bodies and diabetic ketoacidosis. it runs in the family unlike Type I. Maybe a couple of weeks. After time. but remember there is not much family link here. renal insufficiency. * Initial management is diet modification. You cannot live without insulin for a long time. the new vessels are prone to bursting and bleeding which leads to blindness. metformin). HHNS can progress to hyperosmolar coma.72 - . but no acidosis. Ketosis can occur because there is no insulin. It is seen in vitamin D deficiency. * Treatment of hypocalcemia is oral calcium +/. not the macrovascular complications. * Diabetic retinopathy is the most common cause of blindness in middle aged people. Presentation is usually diabetic ketoacidosis. * Identical twins with Type I diabetes has only about a 50% concordance rate. This results from an inflammatory process of the pancreas beta cells causing them to get destroyed and leading to insulin deficiency. Proliferative retinopathy is neovascularization. Diabetes Mellitus * Diabetes is a disease of carbohydrate metabolism. you would need to look that day for proteinuria. * With secondary hyperparathyroidism. These patients may have glucose levels in the 1000s. Most patients present complaining of polydipsia and polyuria. For background retinopathy. the parathyroid glands get activated to constantly dump PTH. This leads to tertiary hyperparathyroidism. Rickets. * DKA usually occurs in young patients with no other comorbid diseases. This has a worse prognosis than diabetic ketoacidosis (DKA) because it occurs in older individuals with comorbid conditions. but non-insulin dependent diabetes mellitus (NIDDM). patient is usually slender and no family history of diabetes. * Symptoms of latent tetany include Chovstek sign where you tap the facial nerve and see an ipsilateral facial twitch. * Renal failure or hypoparathyroidism would cause low calcium and high phosphate. * Type II diabetics can develop hyperosmolar hyperglycemia nonketonic syndrome (HHNS).Study Notes – Internal Medicine James Lamberg 28Jul2010 * Any drop in magnesium levels affects parathyroid hormone. Resistance to insulin decreases with weight loss.g. severe dehydration.decreases.vitamin D if no symptoms and IV calcium if symptomatic. * Type II diabetics are insulin resistant. Patient could get laryngospasm. These patients do hot have any of the microvascular complications. the parathyroid glands start acting autonomously which leads to tertiary hyperparathyroidism. * If patient presents in HHNS or DKA. they develop these at least 5 years later. After many years. and decide if they need an ACE-I. * Definition of diabetes is fasting glucose > 126 for two consecutive visits. * Identical twins with Type II diabetes has a 100% concordance rate. It is difficult to study type II DM because patients have had the disease for a long time but do not know it. you just have to control the patient’s sugar. They do have severe dehydration. * Secondary hyperparathyroidism is caused by hypocalcemia. Background retinopathy is associated with retinal hemorrhages and cotton wool spots on fundoscopic exam. 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). If that does not work you do oral hypoglycemics (e. Some people mistakenly think Type I DM is congenital because patients present as children. you diagnose them with diabetes. Magnesium is needed to secrete PTH and is needed for PTH to act on the osteoclast and the kidney. * Hyperosmolar hyperglycemia nonketonic syndrome (HHNS) is a state of high sugars. Now you cannot suppress the calcium and you have to remove the parathyroid glands. If that does not work you use insulin. This patient would need to go to the ophthalmologist right away to look for retinopathy. You cannot reverse the peripheral vascular disease or cardiovascular complications. but that’s probably years later. no acidosis. * Vitamin D deficiency (secondary hyperparathyroidism) would cause low calcium and low phosphate. * Renal failure patient can get secondary hyperparathyroidism due to lack of calcium. You check their glucose and find it to be elevated. usually 30-40+ years of age. These patients need laser treatment to the eyes or they will go blind. so PTH increase and PO4. brain (neuropathy). they become autonomous. usually older individuals. * 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. The types of microvascular complications are the eye (retinopathy). * Type I diabetics are insulin dependent. Calcium may normalize in the beginning. * Studies show that even excellent primary care physicians miss proliferative retinopathy. parathyroidectomy. It usually does not cause blindness. * We can only reverse the microvascular complications of diabetes with tight glycemic control. Type I diabetes is usually seen in young individuals. So patient with DM must DO NOT DISTRIBUTE . * Type II diabetics are overweight. kidney (nephropathy).

Then give them regular before dinner and NPH before bedtime to carry over until the morning. * Type II DM can get a little NPH once a day or so. then the counter-regulatory hormones kick in and by the time the patient wakes up they are hyperglycemic. Say patient comes in saying their noon blood sugar check is around 300. In the PM. The bottom line is an HgA1c over 8 means they have been poorly controlled for the past few months. use 2/3 NPH and 1/3 of regular (so of the 66. you will decrease the amount of protein in the kidney. * To stabilize any of these complications (ophthalmopathy. If you increased the insulin in this patient at night. use 2/3 NPH and 1/3 of regular or maybe 1/2 of each. 8am sugar is 300.Study Notes – Internal Medicine James Lamberg 28Jul2010 go to the ophthalmologist at least once a year. If patient used 100U over the last 24h prior to hospital discharge. Type I DM need insulin twice a day. 3am sugar of 70 (hypoglycemia). * HgA1c of 8+ correlates to sugars running above 200. midnight sugar of 120. it is just a monitor of disease activity. * Do not diagnose diabetes with an HgA1c level. this is random. * Patients may have complications but show up at your office with normal sugars. 5am sugar is 90. Central cranial nerve that is most affected in diabetes is CN III (ptosis). Now you increase the PM regular insulin. Just understand that a type I diabetic will need coverage throughout the day with short-acting insulin and intermediate-acting insulin. * Patient with diabetes usually presents because diabetes is precipitated by something. so that will kick in around lunch time when given in the AM. Meaning get to normal blood sugar which is < 125. 44 NPH and 22 regular insulin). nephropathy) do tight glycemic control. * Determination of insulin units is based on what they used in the past 24 hours. Which insulin will you increase to cover this (NPH. Somogyi effect is due to rebound from too much insulin use. there is a decrease in functional pancreatic mass after insulitis event. Autonomic neuropathy also causes erectile dysfunction and hypotension. So this is assumed to be from a viral infection (e. To measure glucose control over time. like stress or a cardiac event. * Treatment of Type I DM is insulin. To fix this. Yes. but they do not wake up from the hypoglycemia. patient feels bloated. When you decrease the night insulin. What happens is the insulin wears off at night leading to hypoglycemia. feels full after eating very little. * Mononeuropathy in DM would be a patient with foot drop. neuropathy. Say glucose before bedtime is in the 300s. * HgA1c of 7. * Autonomic neuropathy in DM is associated with gastroparesis. * Nephropathy in DM causes nephrotic range proteinuria > 3g/day but not nephrotic syndrome. * Regular has a peak action of 2-4 hours. During the night you see this example.g. has diarrhea. Another option is to have the patient wake up at 3am a couple of nights to check their blood sugars. Now what do you increase? Increase AM NPH insulin.5 correlates to sugars between 150 and 175. * Type I diabetes occurs due to an inflammatory process. this is called the dawn effect. So patient may get regular insulin then NPH insulin in the morning. wrist drop. Patient will say they are not sleeping well or they are having bad nightmares.5. lisinopril). look at the glycosylated hemoglobin (HgA1c). * Type I DM. * Exception is patient with high sugar in the morning. be worried about somogyi effect and do not increase the night insulin. First. 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 . AM v PM)? Increase AM regular insulin. you could put them in a coma. This can be true high sugar because insulin you gave the day before has worn off. * With morning hypoglycemia. So the treatment of proteinuria or microproteinuria in a DM patient is ACE-inhibitor (e. first line drug is ACE-I. you give 66 units at the next AM and 33 units at next PM. The longer nerve CN VI gets affected in many lesions but in diabetes for reasons unknown CN III is the most commonly affected. give some rapid insulin and some intermediate acting insulin. coxsackievirus) in predisposed individuals. In the AM. then they develop clinical diabetes. the patient with somogyi effect will have normal sugars in the AM but the patient with dawn effect will have even higher sugars. * A normal blood sugar (< 125) over time would correlated to an HgA1c of < 7 or even < 6. NPH onset is around 6-8 hours so it will kick in later in the afternoon. regular. Any patient with hypertension and diabetes. The problem is the second scenario with morning hyperglycemia. Say patient has blood sugar just before dinner is around 300. followed by regular insulin and NPH at night. * To cover a patient throughout the day.73 - .g. If you put the patient on ACE-I. Type I diabetic patient usually have an infection. If patient gets an infection. the somogyi effect or somogyi phenomenon. or cranial nerve abnormality. * Peripheral neuropathy in DM is the stocking and glove distribution (loss of sensation). This looks at sugar over 2-4 months. It does not matter what the patient tells you about their control or their blood sugar at the office visit. Called “law of 2/3rds”. The mass decreases until a diabetic threshold is reached. Break that down into taking most of the insulin in the morning and about 1/3 at night. give the patient AM regular and NPH. Type II diabetic patient may have infection or cardiac event.

a little. * Type II DM treatment starts with diet. Complications of metformin include GI upset and diarrhea (most common). * Hypoglycemia with high insulin is due to a rare pancreatic insulinoma. then insulin likely needed 10 years later. 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.metformin or sulfonylurea. which is an autonomous insulin-secreting tumor. there must also be symptoms. This is called the honeymoon period. Tell the patient to keep exercising and then decrease the morning NPH insulin. UTI) and diabetes is started. 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. symptoms consistent with hypoglycemia. Treatment of the infection (e. so in an overdose you should anticipate hypoglycemia for 24 hours and admit to the hospital.g. They also sensitize the peripheral cells to the effects of insulin. Patient is taking regular + NPH in the morning and evening. and troglitazone are thiazolidinediones (TZDs) which improve glucose use by cells. patients have less complications and do better on this medication. They start working out in the evening before dinner. glucose uptake from the gut. The usual profile of the exogenous insulin taker is someone in the medical profession or lives with someone who is diabetic. then +/. That is because they have residual pancreatic mass and non-clinical diabetes. * Metformin is a biguanides and does not affect the beta cells. Treatment is to eat. improvement after glucose given. * Hypoglycemia in a non-diabetic is initially managed by looking at the body response. frequent meals. So check creatinine to rule out renal insufficiency if DM patient develops hypoglycemia. chlorpropamide. * Sulfonylureas include glyburide. Oral Hypoglycemic Agents * Sulfonylurea have been around for many years. If patient takes too much regular insulin. Another complication that can occur with exogenous insulin takers is development of insulin antibodies. * Hypoglycemia with DM cause occur due to exercise because there is enhanced glucose uptake by muscles without insulin. They are not used due to their side-effect profiles. then +/. then oral hypoglycemics.exenatide or insulin or glitazone. growth hormone. * Most sulfonylureas have a prolonged effect. * DM patient develops new onset renal failure. If you cause a little renal failure with the dye you could increase the lactic acidosis side-effect seen with metformin. pioglitazone.74 - . * Glipizide and glyburide are given once a day or maybe twice a day. then sulfonylurea or insulin or exenatide. They come with clinical evidence of diabetes. or more commonly the patient is taking exogenous insulin. So in a patient with renal failure (common in DM) choose tolbutamide. * Whipple triad: low sugar. this is an inappropriate response. They act on the beta cells to produce insulin. Tolbutamide is not used often because dosing is three times a day. * Normal response of the body to hypoglycemia is to drop insulin down and increase counter-regulatory hormones like cortisol. DO NOT DISTRIBUTE . you can watch and give sugar then discharge.exenatide or insulin or glitazone. * Metformin is a good drug.Study Notes – Internal Medicine James Lamberg 28Jul2010 higher and their pancreatic mass is stressed. All the sulfonylurea drugs are metabolized by the kidney except tolbutamide. then metformin. If the patient has an insulinoma. * Type 2 DM (elderly): low dose secretagogue. If you measure insulin during hypoglycemia and it is normal or high. Metformin acts on the liver to stop neoglycogenesis. * Endogenous insulin is secreted with C-peptide at an almost 1:1 ratio. then switch to simple insulin regimen. Example would be rounding in the AM post-call and someone starts to get wobbly. It also blocks. glipizide. By treating this patient you are protecting the residual functional pancreatic mass and not stressing it. Major action is stopping glucogenesis in the liver. then +/. but notice they feel dizzy and their sugars run in the 50s. so it stops the liver from making sugar. this is an appropriate response to not eating. * Type 2 DM (non-obese): sulfonylurea or metformin first. * Type 2 DM (Asians): glitazone. and glucagon. If you measure insulin and it is zero. not insulin has a longer half-life and patient develops hypoglycemia. Hypoglycemia * Hypoglycemia is not just low sugar in the blood. stop the metformin at least 24h ahead of time. * Rosiglitazone. pneumonia.sulfonylurea. then +/. * Treatment during the honeymoon period is to give the patient low dose insulin. It also facilitates the movement of glucose into muscle. * Acarbose and miglitol are alpha-glucosidase inhibitors that are rarely used because of the severity of their sideeffects (flatulence and bloating). then they call you two weeks later because their sugar level is normal. Patient taking exogenous insulin will have high insulin level but low C-peptide. tolbutamide. * Type 2 DM (obese): metformin first.

* If dexamethasone suppression test is abnormal. * High-dose dexamethasone suppression test is abnormal (cortisol elevated still) now you are stuck. which peaks in the morning. * Dexamethasone is a potent type of cortisol. now check ACTH and if elevated assume lung cancer. After diagnosis. Abnormal response is to give 1mg dexamethasone at night then patient wakes up with high cortisol. * Adrenal adenoma or adrenal hyperplasia or adrenal cancer will cause a secretion of cortisol. buffalo hump. This is a benign disease in that it occurs over a long time (e. At the DO NOT DISTRIBUTE . purple striae). you can exclude Cushing. Now localize the cause (pituitary. hypertension due to mineralocorticoid effect. 10 years) before it is diagnosed. * What if a patient took exogenous sulfonylurea medications? These act on the beta cells to increase insulin and make sugar plummet. * Diagnosis of Cushing syndrome should not involve scanning the patient. purple striae. they will be very hyperpigmented. The difference you know is that patients with lung Cushing have high ACTH with hyperpigmentation and adrenal Cushing do not have high ACTH.Study Notes – Internal Medicine James Lamberg 28Jul2010 * It is important to differentiate exogenous insulin taking from insulinoma. This autonomous secretion cannot be suppressed no matter what you do. So a normal response is suppressed AM cortisol. Next step is get a CT scan or MRI of the pituitary and get neurosurgeon involved. then localize. First screening test is the overnight dexamethasone suppression test. * Small cell (oat cell) cancer in the lung can cause ectopic ACTH secretion leading to Cushing syndrome. * High-dose dexamethasone suppression test is normal (cortisol suppressed) if pituitary adenoma. This patient does not have enough time to develop the typical Cushing appearance. Patients with stress. * So if you see a thin person with hyperpigmentation. diabetes because it is a counter-regulatory hormone. If you give a patient dexamethasone at night. then adrenal lesion is likely so get CT scan of MRI of abdomen and adrenals. It is like the sedimentation rate in temporal arteritis. * Follow-up test is urine 24h free cortisol. * High-dose dexamethasone suppression test is abnormal. Yes it can cause a buffalo hump. If elevated free cortisol. even normal people can have abnormal tests. C-peptide would be elevated as well.75 - . cachectic because of the lung cancer. it could be dispersed cells in the pancreas. and potassium. When you measure hydrocortisone in the morning. * Autonomous aldosterone is secreted and aldosterone holds onto sodium (high Na+). Cushing Syndrome * Excess exogenous cortisol does a lot of things but it depends on how long you are taking the cortisol for. no Cushing. or adrenal). causing hypertension. causing high levels of aldosterone. It is never used as a screening test because you miss all of the semi-autonomous causes (e. This is a malignant disease. Obese patients will have abnormal tests. this patient has some form of Cushing syndrome. It could be either lung or adrenal. Next step would be CT scan of the chest. 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. The main function of aldosterone is to keep salt in vessels. * High-dose dexamethasone suppression test is used for localization. wasted.g. hydrogen ions. * Autonomous adenoma in the pituitary secreting ACTH can cause Cushing syndrome. ACTH is similar to melanocyte stimulating hormone. * Likely the most common cause of Cushing syndrome is iatrogenic. and deals with bicarbonate. to the point where surgery could involve cutting off pieces of the pancreas until the sugar normalizes. in fact they are co-secreted. It is also called Cushing disease because it was in the original patient described (moon facies. looking just like an insulinoma. Because of the huge ACTH secretion. but not specific). maintain vascular tone. lung. nodules in the adrenals that mean nothing. Hyperaldosteronism * Conn disease (rare) is caused by an adenoma in the mineralocorticoid apparatus. Example would be steroid-dependent asthma or collagen vascular disease. * First question is to ask if the patient has Cushing syndrome. Next most common is autonomous ACTH adenoma in the pituitary. it could be Cushing or something else. if the sed rate is normal then the patient does not have temporal arteritis. An insulinoma may be very difficult to locate. Surgery is curative. If ACTH is low. due to very high levels of ACTH. If cortisol is normal. nodules in the pituitary that mean nothing. psychosis. These patients look thin. You will likely find nodules in the lung that are not cancerous. pituitary). do not assume Addison disease.g. This is likely unresectable. Overnight corticotropin releasing hormone (CRH) causes ACTH to increase cortisol. Check that they do not have a form of Cushing syndrome. normal response is to see that enough cortisol is present and not release CRH and ACTH. thus these patients do not have hyperpigmentation. There is a possibility of excision here. If the test is normal. The ACTH is suppressed. It may not be a tumor. you do not pick dexamethasone up on the assay. If there is clinical suspicious for exogenous sulfonylurea use (patient in medical profession or diabetics in family) then check the urine for sulfonylurea levels. This form is autonomous so does not get suppressed.

* Young woman presents with hypokalemia. and elevation is eosinophils in serum for unknown reason. etc. If the adrenal is normal. females are recognized early. no hypertension. Even if the cause is in the pituitary. which is converted to aldosterone. hypokalemia. rather than allowing it to be resorbed into the bloodstream. * 21-hydroxylase deficiency accounts for 90% of congenital adrenal hyperplasia cases and is the only one that could be diagnosed in an adult. magnesium. Signs include hypotension and dehydration. * Primary hyperaldosteronism (Conn syndrome) is a rare form of secondary hypertension. you should see gradually increasing cortisol levels. chloride. you know you are causing secondary aldosteronism. cortisol. There is an unknown escape mechanism where the excess water gets wasted. Thus everything gets shifted to the sex hormone pathway. 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.g. There is a block in the conversion of progesterone to aldosterone. evidence of virilization. then you can get random cortisol levels. and some physicians even question this. over-diuresis. metabolic alkalosis. loss of mineralocorticoids causes low blood pressure. cirrhosis). edematous states (CHF. The low hydrogen ions leaves bicarbonate unopposed. * In this process. This is probably the only time you can get random cortisol levels. it will not get to normal especially in the edematous states. * Exception for rapid ACTH test is sick patient (stressed). Congenital Adrenal Hyperplasia * Cholesterol is converted to progesterone. But. * Gitelman syndrome is a rare inherited defect in the distal convoluted tubule of the kidneys. Measure cortisol levels at zero. * Non-classic form of 21-hydroxylase deficiency can occur. diarrhea. * You would think the patient with increased intravascular volume would have edema. The only difference. potassium is wasted (low K+) and hydrogen ions are wasted (metabolic alkalosis). potassium and hydrogen ions are lost leading to hypokalemic metabolic alkalosis. Treatment is to cut the diuretic dose. cliteromegaly). Also known as renin-dependent aldosteronism. The renin apparatus read this and cranks up the renin. Think about secondary aldosteronism from surreptitious vomiting or use of diuretics to lose weight. most cases are due to idiopathic or autoimmune. * Electrolyte problems are hyperkalemia.76 - .Study Notes – Internal Medicine James Lamberg 28Jul2010 same time. Removal of the tumor is curative of the disease and treats the blood pressure as well. Patients with congenital adrenal hyperplasia are missing enzymes to convert progesterone to aldosterone or cortisol. * Adrenal insufficiency causes increased ACTH so there is hyperpigmentation. * The most common form of hyperaldosteronism is secondary aldosteronism. Males have normal genitalia and can be missed. but they do not. metabolic acidosis. The aldosterone increases sodium in an attempt to get intravascular volume to normal. This occurs in 1 of 100 cases of 21-hydroxylase deficiency. In the United States. Edema is not seen in primary aldosteronism. * Diagnostic testing is to activate the adrenals by giving ACTH. Infections with MAI or CMV in HIV patients can cause adrenal insufficiency. vomiting. and sex hormones. * Treatment is to give mineralocorticoids like hydrocortisone and fludrocortisone because hydrocortisone does not have enough mineralocorticoid action. * All females born with 21-hydroxylase deficiency have ambiguous genitalia (e. very rare. Edema is seen in secondary aldosteronism if they are in the edematous states and not seen in other states. the rapid ACTH test will likely be abnormal so you can get diagnosis there too. * If a CHF patient is on furosemide and gets hypokalemia with metabolic alkalosis. Thus. Think about this as a cause if a hypertensive patient complains of weakness and headaches. metabolic alkalosis. * Rapid ACTH test is negative (no increase in cortisol with ACTH given). It causes the kidneys to pass sodium. It is most common in young adult men. and potassium into the urine. It starts with decreased intravascular volume due to hypotension. Adrenal Insufficiency * Most cases of adrenal insufficiency are due to tuberculosis worldwide. These patients have salt-losing nephropathy due to lack of aldosterone. Bartter syndrome is a rare inherited defect in the thick ascending limb of the loop of Henle. 1hr. which cranks up the aldosterone. is that primary aldosteronism has mainly diastolic hypertension and secondary aldosteronism does not have hypertension. These are both forms of secondary aldosteronism. Treatment is to replace missing hormones. hyponatremia with hypotension. but it won’t stop because it is an autonomous adenoma. The depleted intravascular volume goes back to the renin apparatus. So these patients will complain of weakness. 2hrs. So you are over-diuresing that patient. no edematous states. the rapid ACTH test. give hydrocortisone 10-20mg/day plus fludrocortisone sometimes for mineralocorticoid action. * Primary and secondary aldosteronism both have muscle weakness. Give DO NOT DISTRIBUTE . causing an increase in 17-hydroxyprogesterone. It is also called reninindependent aldosteronism. patient produces some aldosterone and only has symptoms during stress.

regardless of etiology. 10% re-occur. 150/90 sitting up.Study Notes – Internal Medicine James Lamberg 28Jul2010 enough to maintain the blood pressure and electrolytes at normal. hypogonadotropic hypogonadism. E. * Adrenal insufficiency patient going for surgery or gets a febrile illness. * Treatment is first suppress epi/norepi by giving alpha-blockade. * Patients have normal LHRH. 10% are malignant. But if you go in and start playing with pheochromocytoma you will get a large norepinephrine and epinephrine surge. increase maybe up to ten times dose. * Hct > 30-35 is usually asymptomatic. * LHRH causes the release of FSH and LH. * Treatment is surgical excision after blood pressure normalized with alpha blockade. not high output cardiac failure. Symptoms are dependent on the patient too. syncope. * Treatment of pheochromocytoma is surgery. * Chromosomes are XXY or XXXY. This occurs in about 1 in 400-500 births. -------------------------------------------------------------------------------------------------------------------------------------------Kaplan Videos (2001) – Hematology/Oncology with Dr. Older test is VMA (vanillylmandelic acid) and metanephrines. Do not send an incidentaloma to surgery. shortness of breath. * Some patients complain of symptoms like palpitations even with alpha blockade. but the receptors for testosterone production are deficient.g. * Treatment is synthetic LHRH to normalize testosterone. patient is 200/110 laying down. * High output cardiac failure takes months to develop and is not common in the United States since the precursor DO NOT DISTRIBUTE . high FSH and LH. 10% in children. * Young healthy patient might not die until Hct of 10-12. * Klinefelter syndrome patients have a 20x greater risk of breast cancer. If major surgery. Conrad Fischer. which makes testosterone. * Hct < 15-20 is associated with death. Symptoms are most dependent on the severity of the anemia. XXXY has more abnormalities. A tumor is found in the adrenal gland. 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. these are called incidentalomas. The patients blood pressure goes up. If febrile illness. * A patient gets a CT scan for suspected appendicitis. then increase the maintenance hydrocortisone dose. * Pheochromocytoma arises from the adrenal medulla causing increased levels of epinephrine and norepinephrine. * Diagnostic test is urine free catecholamines. 10% extra-adrenal. * Only after you find urine free catecholamines do you proceed to the abdominal CT/MRI. * Patient presents with high blood pressure and you start them on a medication like HCTZ or beta-blocker. * Treatment before surgery also includes IV fluids because they are volume depleted. confusion. Medications include phenoxybenzamine and phentolamine (reversible). Key feature is anosmia (lack of smell). Pheochromocytoma * Pheochromocytoma is a form of secondary hypertension (also primary aldosteronism and renal artery stenosis). eunuchoid features (large waist). Cause of death is myocardial infarction. * These patients present with small testes. confusion. increase hydrocortisone two times dose. is associated with the symptoms of fatigue. Severe illness like pneumonia. Take an older patient with vascular stenosis.77 - . Hct 25-30 symptoms are fatigue. Patient could have complications or even die from this. These patients are volume depleted for unknown reasons. * Most patients (60%) have stable chronic hypertension with pheochromocytoma. If you take random people off the street you will find 15-20% have some non-functional adenoma of the adrenal glands. This is due to a decrease in the release of LHRH. but surgical correction of the underlying disease cures the disease and the hypertension. and there is orthostasis despite the hypertension. thus not the classic presentation. lightheadedness. Consider pheochromocytoma when patient is young. you are using a lot of medication to control their blood pressure. * Rule of 10% for pheochromocytomas: 10% of patients are bilateral. * Secondary hypertension is less than 5% of all hypertensive patients. This would be expected in pheochromocytoma since alpha receptors are open. increase to 75-200mg/day hydrocortisone. malaise. * Treatment is testosterone. do nothing. * Hct 20-25 symptoms are shortness of breath on exertion (dyspnea) due to lack of oxygen carrying capacity. MD -------------------------------------------------------------------------------------------------------------------------------------------Anemia * Anemia. Hypogonadism * Kallmann syndrome is isolated gonadotropin deficiency. * Hct 15-20 symptoms are lightheadedness. What do you do next? This is likely an incidentaloma because BP is normal. The patient’s blood pressure is normal. and anosmia. they may die at an Hct of 24 or become symptomatic at 28. malaise. Only if the alpha blockade is adequately controlling the blood pressure could you add a beta-blocker to control symptoms.

myopathy. If low it is microcytic. zidovudine. refractory anemia with ringed sideroblasts. mercaptopurine). high is macrocytic.g. * To have AML. * Iron deficiency anemia: low ferritin (most specific). say you get hemochromatosis from iron overload with iron deposits in organs (liver. Hg A2 is two alpha chains plus two delta chains. * Dysplasia (e. Four gene deletion patients are dead. We cannot treat this form of hemochromatosis (secondary to thalassemia major) with phlebotomy. thus increased A2 and F. it comes down to hypochromic microcytic anemia with normal iron studies. * Thalassemia major requires a unit of cells every 2-4 weeks. * Microcytic anemia (TICS): thalassemia. * Anemia of chronic disease: high ferritin. Half the volume of stool is cells. You can live without your brain functioning but cannot live without your heart functioning. chronic disease anemia. skin. * Treatment for thalassemia major is blood transfusion every few weeks. these symptoms are from alcohol. thus is the most common drug cause of macrocytic anemia. What do you do first to establish a diagnosis? Answer is peripheral smear. low TIBC. So in alpha thalassemia there are no beta chains. Single gene deletion patients are normal so not likely to be seen in clinic. but the new cells will be more deficient than the old cells. and refractory anemia with excessive blasts are all the same disease. colon polyps. so you will continue to have bowel movements even if you do not eat. cardiomyopathy. high TIBC.g. Who cares though. * Latest and greatest treatment for iron deficiency anemia is iron. Hereditary deficiency in pyridoxine metabolisms. These will all look hypochromic and microcytic on peripheral smear. Genetic counseling does not mean do all the karyotype testing. and carbon monoxide poisoning (decreased oxygen delivery). Refractory anemia. So one little mL contains all the iron you need for a day. * Most normal iron loss is through the GI tract. * Mean corpuscular volume (MCV) tells you the size of the RBCs. * Next step in management is iron studies. Associated with lead poisoning. testicles). * Treatment of iron overload in thalassemia major is deferoxamine. * Unit packed RBCs has 1mg/mL of iron. alcohol. Hg A is two alpha chains plus two beta chains. There are about 5mL in a teaspoon and 15mL in a tablespoon. * Ferritin is the storage form of iron. * Thalassemia anemia: normal iron studies.Study Notes – Internal Medicine James Lamberg 28Jul2010 causes are usually managed. methotrexate. * Hematocrit (Hct) is found to be low. chronic myelomonocytic anemia. Microcytic Anemia * Iron deficiency anemia is usually from blood loss. * Macrocytic anemia: B12 deficiency. * Normocytic anemia: hemolysis. pancreas. iron running out. What is the next step? Answer is look at cell size (MCV). * Sideroblastic anemia: high iron (only microcytic anemia with a high circulating iron level). cervix) is premalignant. * Stroke is also not the cause of death in anemia. so treatment with vitamin B6 can help them. Hg F is two alpha chains plus two gamma chains. There is no real mechanism to get rid of excess iron. 5-6mg/day when pregnant. Electrophoresis tells you what type of thalassemia.g. benign prostatic hypertrophy) is not premalignant. sideroblastic. iron deficiency anemia. fibrocystic breasts. If the smear is abnormal showing DO NOT DISTRIBUTE . MCV is 110 (normal 80-100). RDW will be increased because the newer cells are smaller. Hct is 28. Hyperplasia (e. * Latest and greatest treatment for anemia of chronic disease is to treat the chronic disease. Two gene deletion is mild anemia and three gene deletion is moderate anemia. liver disease (liver cannot metabolize fats/lipids and they stick to the RBCs). 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. you can live by being stupid and in love but not intelligent with no love. Maximum absorbable is 3-4mg/day. or normocytic. * Treatment of thalassemia minor (thalassemia trait) is do nothing. You only need 1mg/day of iron when not menstruating. 23mg/day when menstruating. Total iron binding capacity (TIBC) is unoccupied sites. it just means tell the patient to avoid having sex with people who has the same genetic problems that they have (e. If the smear is normal. Alcohol can also cause dementia. Reticulocytes are usually larger. genetic counseling. peripheral neuropathy. * Left ventricle cannot distinguish between anemia (decreased oxygen delivery). blood loss.g. folate deficiency. heart. Most sensitive test is bone marrow looking for stainable iron stores. Unit packed cells of 350mL is enough iron for a year. coronary artery stenosis (decreased oxygen delivery). which helps you determine the etiology. family planning).78 - . but this is not the first test. You could treat hereditary hemochromatosis or polycythemia vera with phlebotomy. medications (e. Myelodysplasia (MDS) is premalignant for leukemia (AML). Yep. these are myelodysplasia with a certain percentage of blasts. you need 30% blasts. * Alcohol directly suppresses bone marrow.

Sign nonspecific tissue damage. So B12 deficiency can occur without neurologic problems. But you do not have to have one before the other.6F. Alcohol. and infection predispose sickle cell patients to sickling. as he states. you have to order both the folate and B12 levels. Hemolysis * Causes of hemolysis include sickle cell disease. You note no lower extremity ulcers (a complication of sickle cell). So for exchange transfusion you get rid of half of their (homozygote) blood and replace it with normal blood. * All forms of hemolysis have normal MCV (80 to 100). * All present with high LDH but this is nonspecific and increased in anything that causes cell destruction. * Folate treatment can fix the hematological problem of B12 deficiency. We also know that patients can sickle without any of those things. * Hematologically. * B12 deficiency has neurologic problems.” His temperature is 98. CBC. lymphoma. 47yo man comes to the Emergency Department with a history of sickle cell and complains of terrible pain in the chest. RR of 12. and drugs can make cells macrocytic (large cells) but not megaloblastic. Schilling test is only done when you know you have B12 deficiency and you want to know the cause (bacterial overgrowth blind loop syndrome. but not the neuro problem. it goes up in B12 deficiency. * 21yo patient asks about testing because his father gets treated for sickle cell. * Reticulocyte counts will be high.79 - . there is no difference between folate deficiency and B12 deficiency. * Treat the above 47yo patient with oxygen. Peripheral smear is what you do for this patient. then you know it is due to folate or B12. Hemolysis is the only one that can be acute. How should you manage this patient? * Most accurate or specific test is electrophoresis for sickle cell. “painful sickle crisis. and thighs. Treatment of B12 deficiency is B12. Patients with sickle cell trait will have a normal smear. A few hours later he is worse with blurry vision because the sickle cells have reached his eyes. He is asking for narcotics to treat his. hereditary spherocytosis. If you have an acute situation. The patient has never had symptoms. no gallstone history (bilirubin). tissue destruction (muscle. leukemia. The smear can tell the difference between sickle cell trait (heterozygous) and disease (homozygous). dehydration. glucose 6 phosphate dehydrogenase (G6PD). He says there is no test to disprove pain and that you cannot prove he is not feeling horrible pain. Peripheral is the most common. How do you treat this patient now? Treatment is exchange transfusion. subacute combined degeneration of the cord which accounts for the vibratory sensation problems and looks like tabes dorsalis. Neurologic problems are memory loss. rhabdomyolysis sometime. Microcytic or macrocytic all have to be chronic. * We know that hypoxia. autoimmune. fluids. You tell him you think he is not in pain. * Heterozygote sickle cell patients are about 40-50% sickle hemoglobin and 50-60% normal hemoglobin. * Increased bilirubin can be seen in hemolysis. * Sickle cell in 1 of 400 African Americans and 8% have the trait. not hemolysis because no nuclei. which basically turns them into a heterozygote. pain medication. not history of osteomyelitis (most common staph aureus. look for normocytic anemia. you can get any neurologic issue that you see on a neuro exam. fluids. CNS disturbances. * Say you gave the 47yo patient oxygen. 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. liver disease. * Hyperuricemia can only occur in cells that have the purines and pyrimidines of nuclei. brain. You could see that in tumor lysis. and priapism due to infarction by sickle cells of the prostatic plexus of veins that drain the penis. acidosis. and bilirubin do not tell you if the patient has sickle cell. If you see hypersegmented polys. folate deficiency does not. myeloma. * Methylmalonic acid used with equivocal B12 level. O2 Sat 100% on room air. The low threshold for antibiotics is because these patients are immunocompromised due to function asplenia. * Hydroxyurea is used for prevention of sickle cell crisis.Study Notes – Internal Medicine James Lamberg 28Jul2010 megaloblastic cells. most common pernicious anemia. salmonella only happens in sickle cell). no aseptic necrosis of the femoral head. rare Diphyllobothrium latum fish tapeworm). * Only B12 and folate can make cells megaloblastic (hypersegmented). These patients can die from pneumococcal or hemophilus sepsis very quickly. You cannot get thalassemia or iron deficiency in the acute setting. decreased vibratory sensation. DO NOT DISTRIBUTE . lung). and pain medications. reticulocyte count. blood. paroxysmal nocturnal hemoglobinuria (PNH). * Give sickle cell patients antibiotics without obvious signs of infection if they simply have a fever or leukocytosis. But. peripheral neuropathy. and antibiotics. good sensitivity but poor specificity. sickled cells occur in the disease. back. * Any patient with neutrophil count < 500 and a fever should get antibiotics (neutropenic fever). * Treatment of folate deficiency is…wait for it…folate. Posterior columns also contain large two-point discrimination pain fibers. In reality. like leukotriene antagonists for asthma prevention.

* Osmotic fragility test swells the cells a little bit causing lysis. Testing shows sickle cell trait. * Autoimmune hemolysis should be considered as the cause when you have signs of hemolysis and a history of autoimmune disease. Most common oxidative stress is infection. Leukemia * Forms: Acute myelogenous leukemia (AML).80 - . We know acute leukemia can be caused by chloramphenicol. Answer is renal disturbance such as hematuria. * Acute forms are immature cells. Spherocytes are the opposite of a target cell. this is an acute drop in cells that is not blood loss. measuring a G6PD level will show a normal level. cephalosporins. * Acutely. This cell travels to the spleen and the spleen takes little bites of the iron. and chronic lymphocytic leukemia (CLL). * Drugs that cause autoimmune hemolysis penicillins. * Coombs test differentiates autoimmune hemolysis from other forms of hemolysis. dapsone use. * G6PD deficiency associated with Mediterranean descent. * What is the normal drop in hematocrit with a sickle cell crisis? Answer is none. avoid certain drugs. This is because the most deficient cells are destroyed leaving the normal cells behind. * 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. benzene use. * G6PD deficiency is the only hemolysis cause that has an enlarged spleen because it is chronic. Autoimmune hemolysis has spherocytes as well on peripheral smear. radiation. the problem is not the cell it is the spleen. Like all other forms of hemolysis. The malarial also does not recognize the cell as well because it is lacking certain receptors. Autoimmune is the only one that is Coombs test positive. kills you slower (6-12 years even without therapy). 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). In asymptomatic patient. low or dysfunctional white cells gives high fever and infection. eventually converting into a sphere. like SLE. certain drugs. rifampin. but that could happen. found on routine screening. nutritional DO NOT DISTRIBUTE . so they see the hemoglobinuria in the morning. * Treatment is to remove sources of oxidant stress. don’t eat fava beans. Half the time it is idiopathic. thrombocytopenia gives bleeding. so that is the treatment. * Sodium metabisulfite test is a screening test for sickle trait that is sometimes used. * Presentation for AML and ALL is based on the severity. Mnemonic: It is like becoming allergic to your own blood. etc. * Causes of pancytopenia include cirrhosis and portal hypertension causing hypersplenism as the spleen can sequester all three cell lines. Patient asks what that means for him. chloramphenicol). kills you quick (as short as 6-12 weeks). The problem is when the spherocyte meets the spleen and cannot get through hemolysis occurs. Thus. leaving bite cells. It is an old test. so you can lose 20-30% of your hematocrit via reticulocytes over the next few days. * There is no known cause for chronic leukemias. any primary or metastatic cancer. Thrombosis of large vessels (DVTs. The same drugs cause allergic interstitial nephritis. They can be used to tell you that you have G6PD deficiency. it just removes the cause of hemolysis. primiquin use. The antibodies attach to the RBC and take out little bites. lymphoma. where metabisulfite is added to blood. * Spherocytosis is diagnosed with an osmotic fragility test. chronic myelogenous leukemia (CML). radiation. sulfa drugs. * The problem is not that you have spherocytes. So the smear can tell you if someone has the disease but cannot help you differentiate normal from crisis. acute lymphocytic leukemia (ALL). think of the drugs people are generally allergic to. methotrexate. fava beans. a CBC and peripheral smear will not be helpful. carbamazepine. kidney infections. Splenomegaly takes time. If it keeps recurring. autoimmune (SLE). portal hypertension. Anemia gives malaise. it binds up the oxygen and causes localized hypoxia to provoke sickling. Wait for a couple of months then do a G6PD level. it does not happen right away. Splenectomy does not remove the spherocytes. pancytopenia. Chronic forms are more mature cells. * Treatment of bad autoimmune problems is steroids. Also some genetic counseling. * Homozygous sickle cell patients can have sickle cells even without crisis. portal vein thrombosis) can occur but we do not know why. do splenectomy. bone marrow depressing drugs (most common alcohol. isosthenuria. which has a compact hemoglobin and a big floppy membrane. Less common worries would be getting sickle cell while climbing Mount Everest. * Parvovirus freezes the bone marrow. * Paroxysmal nocturnal hemoglobinuria (PNH) presents with just that complaint. * Oxidized iron in a RBC (precipitated oxidized hemoglobin) is Heinz bodies. Most people do not get up to urinate at night.Study Notes – Internal Medicine James Lamberg 28Jul2010 Test of choice here is electrophoresis. aplastic anemia. sulfa drug use. * PNH responds to steroids for unknown reasons. Diagnosis cannot be made on history. they carry oxygen and CO2 just fine.

* CML M3 is treated with all-trans retinoic acid (vitamin A derivative). So these cells look normal but have abnormal function. * CLL Stages: 3 – anemia. * With recurrence after chemotherapy agents. You wouldn’t use fluconazole to try to kill bacteria. vincristine. anemia. Marrow transplant is an option. eosinophils. and prednisone. Lymphocytes have T-cells and DO NOT DISTRIBUTE . Then you do another round and remove 99.000 lymphocytes particularly because you need to get a bone marrow biopsy for that. which causes DIC. low in 1/3. Aplastic Anemia * CBC has WBC.9% of leukemia cells in the body (remission induction). pro-myelocytic. * Treatment for AML is daunorubicin and Ara-C (cytosine arabinoside). 4 – low platelets. * CLL differential will be 90-95% lymphocytes. Philadelphia chromosome codes for tyrosine kinase. then look for Philadelphia chromosome. marrow-invading infections (TB. These patients are generally too old for bone marrow transplants. CML cell on smear does not look different from normal neutrophil. This is a 10-12yr survival. Yes you may see some smudge cells with CLL as you are putting down the cover slip it smudges the fragile cells. but there were so many cells to start with that three rounds are needed. * The 7-8 different types of acute leukemia (M0-M7) cannot be distinguished from history and initial tests. Acute leukemias are high in 1/3. 1 – lymph nodes. This seems like a huge change. This leukemia is a little different because you can give CNS prophylactic therapy with intrathecal methotrexate. The same goes for leukemia drugs. One round of daunorubicin and Ara-C takes out 99. Medical therapy is Gleevec (imatinib mesylate). * Side Note: 25% of the population feels “chronic fatigue” at any given time. Marrow transplant is an option. * You made leukemic cells today. What is the next step? Answer is differential. “a little tired. * CLL Stages: 0 – increased WBC. lymphocytes. Interferon is another option as it makes the Philadelphia chromosome negative.9% of what was left (consolidation). * An enlarged spleen is most characteristic of CML. Average age of man in United States is 76. If all the cells were not removed. * Treatment for CLL is chlorambucil and prednisone. The differential shows 93% lymphocytes. no therapy. * Side Note: Treatment of multiple myeloma is melphalan and prednisone. virus). they begin to divide and 6 months later you have leukemia again at the brink of death. Results from routine tests from a previous visit show a WBC of 75. There is no equivalent of Gleevec for CLL so we’re stuck with carpet bombing via chemotherapy. What is the diagnosis? CLL. * Patient at clinic for routine exam and found to have high white count. This is a 1-2yr survival. cALLa seen in ALL (common ALL antigen). * The difference between all those causes and acute leukemia is blasts. Retin-A for acne is cis retinoic acid. * You wouldn’t use metronidazole to try to kill viruses. so this drug specifically inhibits the tyrosine kinase. * M3 also has Auer rods. * Chronic leukemias always have high white counts. like stepping on a jelly donut. * Patient who is 50-60yo with CLL and advanced stage disease (hypersplenism. How do you distinguish CML from CLL? * CLL cell on smear does not look different from normal lymphocyte. * You didn’t want to get a Philadelphia chromosome on the patient with 62. When you see the high neutrophils. not at state 1 which is lymph nodes. * Exception is M3. fungus. a silver bullet. 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. The ultimate goal of chemotherapy is to remove so many cells that your body can eliminate what is left. We would call this a cure. do a round of chemotherapy to remove 99. myeloperoxidase. They all present the same so no real need to know them unless you are an oncologist.000 white cells. * Treatment for CML is bone marrow transplant if donor. * For ALL and AML. Then you stop so the patient doesn’t die. This is how you pick up CML and CLL. Your immune system eliminated them. Japanese women live the longest to age 84. then you are more confident it is CML which is associated with Philadelphia chromosome. You wouldn’t use acyclovir to try to kill fungi.000.9% of what was left (maintenance). CML differential will be 90% neutrophils/polys. platelets. Now what? Answer is do nothing.9% of cells. RBC. * 73yo man comes to your office for advice on diarrhea prophylaxis prior to a trip to Mexico.Study Notes – Internal Medicine James Lamberg 28Jul2010 deficiency (B12 and folate). Then a third round to remove 99. This is why we transplant immediately if a donor exists. * High white count with nearly all neutrophils on differential.” * Patient found to have 62. normal in 1/3. * Wait.81 - . thrombocytopenia) should be treated with chlorambucil or fludarabine. The others are indistinguishable with initial tests. Fludarabine if that does not work. * Treatment for ALL is daunorubicin. This is no good because these patients die. do a bone marrow transplant. and they have the same initial therapy. but hematologist/oncologists call this a sustained remission. * CML can convert to ALL in about 20-25% of patients (“blast off”). WBC has neutrophils. Average survival for this guy is 10-12 years.

where patient is not immunosuppressed as much. * If your T-cells were injected into a horse. cells are like “yo buddy we’re the eosinophils you’ve always been with” and T-killer cells is like “uhh. * Staging is important. give medications (ATG. * How do you determine if local? You could start with CXR. Give this to the patient. Plasma cells are 5%. * Most common complaint is unexplained bone pain. * Aplastic anemia can be from drugs. * Myeloma is > 10% plasma cells for diagnosis. No anemia or renal dysfunction. If you radiate her neck and she has disease in her pelvis. * A needle biopsy smear will look normal. it’s a trick you want to kill me. * What drugs would you use to suppress T-cell function? Cyclosporine.g. I’m here to kill you” but body says “don’t bother me. Stage IV: Diffuse disease. no humerus fracture from leaning against something. cyclosporine). the horse would make antibodies against them. she is at stage IIb. I’m fighting another antigen. autoimmune (for unknown reasons). laparotomy (e. If chest CT negative. It is difficult to transplant patients with myeloma because this occurs in older individuals and the transplant itself can kill the patient. same side of diaphragm. drug. * Treatment if chloramphenicol. B is symptoms of fever. CLL and lymphoma are very similar. * Immunoglobulins made against a single antigen (monoclonal). * Treatment is melphalan and prednisone. * Early stage (I to IIa) is radiation and late stage (IIb to IV) is chemotherapy. specifically suppresses the T-cells. well I’m going to kill you first!” The T cells start to kill the rest of the marrow. T-cell subtypes range from CD1 to CD134 thus far. Plasma cells also making Bence-Jones protein (immunoglobulin parts that end up in urine). fever. but this is just to reduce the number of cells. Treatment is stem cell transplant. * Older patient who coughs and causes ribs to break. * Hodgkin disease 80-90% of the time presents in stage I or II. Older people do not recover well when made pancytopenic and neutropenic with chemotherapy prior to marrow transplantation. platelets? What is this. abdominal and pelvic CT. * Man comes to you because his total protein was found to be elevated on routine visit. 1% of these patients go on to myeloma but we cannot determine who does. So she would get chemotherapy. * CXR negative. which is aplastic anemia. No Bence-Jones protein in urine. There is some leeway here. 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. * Most of the time with aplastic anemia it is autoimmune. Normal uric acid level. This disease is called monoclonal gammopathy of undetermined significance (MGUS). You need to see architecture. * Non-Hodgkin disease 80-90% of the time presents in stage III or IV. “Hey buddy. whoa. What do you do next? * Answer is no treatment. * So one day the T-killer cell wakes up and says. * Treatment for autoimmune aplastic anemia is bone marrow transplant if you are young and have a donor. Excisional biopsy comes back positive for Hodgkin lymphoma. Patient says he does not have bone pain. such as in marrow. osteoclast activating factor (OAF) which goes to bones and seeps calcium into serum. DO NOT DISTRIBUTE . they are abnormal lymphocytes that look relatively normal on smear. bone marrow comes back. no pathologic fractures. What is the best thing to do next? Answer is staging because treatment is based on stage. Pneumococcus shows up in the body. T-killer. she is going to die. reset the bone marrow. alcohol. weight loss.82 - . This implies a worse prognosis. This is anti-thymocyte globulin (ATG). Think myeloma with non-traumatic bone pain in old person. Calcium level is normal. rolls over in bed and gets broken bone. no you’re not. weight loss. a defect in the T-cell. then could do chest CT. Lymphoma * 32yo woman presents with neck mass. Myeloma * Plasma cells are making IgG and IgA that are detectable on serum protein electrophoresis. then abdominal and pelvic CT. * Stage I: One group of lymph nodes.Study Notes – Internal Medicine James Lamberg 28Jul2010 B-cells. how did you get into my marrow? T-killer cell develops homicidal ideation. uric acid (hyperuricemia). benzene. * Stages have A and B. night sweats. bone marrow aspiration (lymphangiogram was old test). alcohol. in spleen not seen on CT). then you can radiate a local lymphoma. It is so busy creating antigens and fighting this unknown/nonexistent thing that real infections run rampage. Needle biopsy is not good enough. Stage II: Two groups of lymph nodes.” The only person who can see this magic antigen is the body. used in kidney transplantation. no salt and pepper head. * Stage III: Both sides of the diaphragm. If all of these are negative. who are you guys? B-cells. You do an electrophoresis that shows a monoclonal spike. radiation use is to stop the offending agent. What would you do next to determine the diagnosis? Answer is excisional biopsy. with plasma cells delusional creating antigens against some antigen. chest CT. sweats. If no donor. * Testing for localization: CXR. T-cells knocked out. If it showed mediastinal and hilar lymph nodes for this 32yo with a neck mass.

Then get a von Willebrand factor level. normal PTT. Factor XIII helps preserve the clot. * In order for platelet and endothelium to stick to each other they need vWF. * Treatment of von Willebrand disease is desmopressin (DDAVP). It is not hemophilia because she is a woman. * 26yo with platelet-type bleeding. This rapidly brings up the vWF level. with factor-type and platelet-type bleeding. Tissue plasminogen activating factor (tPA) so that the plasminogen turns into plasmin and then the plasmin chops up the fibrin linked clot. * Radiation of local disease results in a cure 90% of the time. Factor VIII and vWF sit in the endothelial lining. weight loss. * DIC has low platelets. give factor VIII replacements because it comes with some von Willebrand factor (vWF). hematoma in muscle) or platelet bleeding (superficial like epistaxis. fever. What is the most likely diagnosis? This is platelet-type bleeding with a normal platelet count.000) because bleeding time will always be abnormal. * Glanzmann thrombasthenia and Bernard-Soulier syndrome are rare. leading to good clotting. MOPP. factor-type bleeding. Pelvic CT scan is positive for lymph nodes consistent with lymphoma. Bleeding time is a test of platelet function. To see if there is functional vWF. This is idiopathic thrombocytopenic purpura (ITP). * First thing to do with a bleeding question is determine the nature of the bleeding before you look at the labs. * Megakaryocytes are precursors to platelets. so increased in ITP. PT is normal. Adriamycin gives cardiac toxicity. von Willebrand disease. * Factor VIII antigen (vWF) travels bound to the factor VIII coagulant portion (hemophilia). Is this factor related bleeding (deep like hemarthrosis in joint. prolonged/normla PTT. * Busulfan and bleomycin cause pulmonary fibrosis. If DDAVP does not work. Vincristine and vinblastine causes peripheral neuropathy. but you need a bone marrow biopsy to see these. prolonged PTT. Testicles are more vulnerable to this effect. but enough so the artery is open. factor-type bleeding. Fibrin split products gets split off from fibrinogen to activate it to fibrin. the platelets do not stick to ristocetin. They are made with E. * They tell you the spleen is normal to rule-out splenic sequestration. where it is made and stored. DO NOT DISTRIBUTE .83 - . normal platelets. If that doesn’t work. * Factor replacements (VIII. you could look at the empty beer bottles (D-dimer) or the bottle caps that were split off (fibrin split products). night sweats. Then you time the bleeding. 1% will develop aplastic anemia. What is the next test for diagnosis? Answer is antiplatelet antibody test. PTT normal. increased PT. * If you wanted to know how many beers someone drank. This is the ristocetin test (artificial endothelial surface). * Most common side effect of chemotherapy (CHOP. so do not do a bleeding time if the platelet count is low (< 50.000. Her prothrombin time is normal at 11s. Bleeding Disorders * 26yo woman presents with epistaxis and petechiae. Cisplatin causes nephrotoxicity and ototoxicity. So do bleeding time when you see platelet type bleeding with a normal platelet count. normal platelets.Study Notes – Internal Medicine James Lamberg 28Jul2010 * Treatment of non-Hodgkin lymphoma is CHOP. fibrin come in and cross-links the clot. * How do you do bleeding time? You put on a BP cuff to occlude the veins of the arm. thus it is not used much. normal platelets. you need an artificial endothelial surface. platelet-type bleeding. coli and recombinant technology. so in the 26yo patient so most likely von Willebrand since it is the most common hereditary coagulopathy. * TTP is associated with renal failure and hemolysis. vagina)? * Hemophilia: normal PT. Excision biopsy shows Reed-Sternberg cells. PTT is prolonged at 52s. platelet count low. Hepatitis B vaccine is made this way too. gums. ABCD) is sterility in 95% of patients. increased PTT. IX) are clean because they are no longer pooled blood products. Fibrin is broken to D-dimers (fibrin parts) by plasmin. * After the initial clot is formed via vWF with platelets and endothelium. * Von Willebrand disease: normal PT. Cryoprecipitate is pooled blood products and can transmit disease. * Treatment of Hodgkin lymphoma is ABVD/MOPP. skin. 1% a year develop AML. platelet count of 217. mucosa. * Desmopressin releases sub-endothelial stores of vWF. then you might give cryoprecipitate. The spleen is not enlarged on exam. If you have platelets and ristocetin with vWF present they will stick. * Say you have platelet-type bleeding with normal platelet count. What would you do next in the management of this patient? Stage is IIIb so do chemotherapy with ABVD/MOPP. If vWF is not there. Then you take a razor blade and cut the patient. * 32yo woman with a neck mass. Why don’t we just chemo everyone? Side effects. * Vitamin K deficiency: prolonged PT. What is the treatment? Steroids. so it is not unusual to see prolonged PTT in von Willebrand disease. What is the next step in management with the assumption of von Willebrand? Answer is bleeding time (prolonged). Cyclophosphamide causes hemorrhagic cystitis. * It is not vitamin K deficiency because PT is normal.

She denies back stiffness or back pain. not ECG. * Labs looking for anemia of chronic disease (MCV low normal. this is 20 joints involved so polyarticular. calor (hot). The surgeon sends the patient to you because the PTT is prolonged. * This is very much like autoimmune hemolysis. it has a half-life and will decay. myasthenia crisis. a PE before. * Diagnosis is not made by a single serologic test being positive. She has stiffness for two hours every morning since these symptoms started and the symptoms improve as the day progresses. an autoimmune disease. Not CXR. high ESR. MCPs. Steroids for both. If you give vitamin K and the patient gets better it was vitamin K deficiency. DO NOT DISTRIBUTE . * In RA. liver function. loss of appetite. On exam the wrists. * The only hypercoagulable state that has an elevation in bleeding labs (PTT increased) is lupus anticoagulant. Arthralgias are joint aches. Glucose could be up as a complication of steroids. loss of energy have corresponding inflammatory laboratory results such as anemia of chronic disease. What is the next step in management? IV Ig or RhoGAM. loss of joint space and inflammation. * 26yo woman with platelet-type bleeding. C1-C2 joint is the only area of the spine that can be involved in RA. meaning RA with positive rheumatoid factor. normal PT. high platelet count. PTT is normal. subdural hematoma. DIPs are almost never involved. subarachnoid hemorrhage as well. She also has pain in her wrists. Increased reticulocytes are like increased megakaryocytes. Another manifestation is pulmonary nodules (Caplan syndrome).Study Notes – Internal Medicine James Lamberg 28Jul2010 * Treatment of ITP is steroids. What do you do next? * Hemophilia presents as a child that slides into base playing baseball and gets a hemarthrosis. normal platelets. Psoriatic arthritis is similar to RA but psoriatic arthritis affects DIPs. although it can be seen in other disease. Thus. Thus the platelets are not processed. * Rubor (red). kidney function. She points to all her proximal interphalangeal (PIP) joints as well as the metacarpal phalangeal (MCP) joints. increased platelet count. weight loss. As a side point. PT is normal. platelet count is low. So this patient has ITP and is bleeding into her brain and bowel. Pyloric stenosis because you’ll see it again [the food]. * Serologic tests include rheumatoid factor (IgM antibody against IgG). epidural hemorrhage. give FFP. PEs. * “Memorized learning or non-understood learning is one of two things. Classic MCP and PIP involvement and the joint involvement is symmetric. * Lupus anticoagulant: Elevated PTT. Giving IV Ig stuffs up all the Fc receptors on the macrophage. radioactive material. usually presents in young adults. night sweats. dolor (pain) for joints inflammation. MD -------------------------------------------------------------------------------------------------------------------------------------------* Pay attention to the number of joints involve. and other acute phase reactants like C-reactive protein (CRP). * What imaging tests would be abnormal in this patient? Hand joint x-rays showing erosions in the joint space. TIBC low. She has fatigue and low grade fever (think generalized inflammatory condition). and PIPs are red and swollen on both hands. History of recurrent abortions. glucose level. Fe low. Goodpasteur. Normal electrolytes. high PTT. high CRP. high sedimentation rate (Sed rate). Or.” * Macrophages bring the platelets that have antiplatelet antibodies and drag them to the spleen for processing. * Plasmapheresis sounds like a good idea. * Treatment of lupus anticoagulant is to replace factors. * At least 70% of patients are have seropositive RA. If patient recurs then do splenectomy. normal platelets. not CT scan of head. He did have a DVT three years ago and last year. can get fibrosing changes causing restrictive disease. * If a joint is swollen and/or fluid filled compared with other joints. Rheumatoid Arthritis (RA) * 26yo woman with no prior medical history presents with a three week history of joint swelling and stiffness. platelet count is normal. There is a circulating antibody (Guillain-Barré. DVTs. they only help confirm diagnosis. this is the quickest way to raise the platelet count. not inflammation. -------------------------------------------------------------------------------------------------------------------------------------------Kaplan Videos (2001) – Rheumatology with Dr. * What is the most likely diagnosis in the 26yo woman? Rheumatoid arthritis.84 - . but usually not necessary. The patient has no bleeding history and has had prior surgeries without event. * Constitutional symptoms are fever. Test for autoimmune hemolysis is antiRBC antibody (Coombs) versus antiplatelet antibodies for ITP. ITP) why not get rid of it? Just not necessary in most cases. if labs do not change it is liver disease. * Morning stiffness is a classic disease marker for rheumatoid arthritis. * 62yo man has a prostate mass and is going to get a biopsy. ferritin normal or high because ferritin can act as an acute phase reactant). * Fresh frozen plasma (FFP) has no platelets. * Extra-articular manifestations of RA include splenomegaly and neutropenia (triad is Felty syndrome). do an arthrocentesis. The distal interphalangeal (DIP) joints are not involved. 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. Splenectomy is the steroids fail and the patient recurs. not x-rays of lumbosacral spine. PT is normal. * Liver disease has very high PT. Asher Kornbluth. * Ratio is about 3:1 women to men for RA. melena.

Study Notes – Internal Medicine

James Lamberg

28Jul2010

* 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.

DO NOT DISTRIBUTE

- 85 -

Study Notes – Internal Medicine

James Lamberg

28Jul2010

* 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).

DO NOT DISTRIBUTE

- 86 -

Study Notes – Internal Medicine

James Lamberg

28Jul2010

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.

DO NOT DISTRIBUTE

- 87 -

so you cannot use the same dose. you cannot make a diagnosis of the cause of monoarticular arthritis. A day later they spike fevers still and have high WBC on arthrocentesis. Crystal is blue when parallel to the slow ray of the compensator. So what are you going to do? NSAIDs now and repeat every few hours. This is probably nafcillin-resistant staph. Treatment is nafcillin or vancomycin if allergy. and very painful. * Pseudogout crystals are calcium pyrophosphate which is positively birefringent rhomboid-shaped. * Ankle tap shows WBC of 40. A WBC < 5000 is more likely traumatic than gout or septic. safe in pregnancy. * Another option is colchicine repeatedly until there is decreased pain. Best choice though is oral NSAIDs. but that does not mean it occurs at the time of their gouty attack. Staph arthritis associated with IV drug abuse. * 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. the patient doesn’t care about a diagnosis. you have the wrong bug or the wrong drug. like Lyme disease. Causes include sepsis and crystal-induced. * Gonococcal urethritis can be treated with normal dose IM ceftriaxone. even painful swollen hot red. Now what do you do? Answer is polarizing light microscopy. * There are many other causes. infected central line. Examination shows red swollen ankle with evidence of an effusion. What is the first step in the evaluation of this patient? Answer is tap the joint. Do examination of joint fluid under polarizing light microscopy (for crystals) or do a Gram stain and culture. DNA broken down to purines to uric acid. But. What is this consistent with? Gout or pseudogout. They have urethritis with discharge followed by a flulike illness with constitutional symptoms then perhaps a fleeting rash (petechial.g. * Gonococcal arthritis associated with sexual activity. The patient should feel better within the first dose or two.000. A serum uric acid that is normal or low should not rule out the diagnosis of gout. Negatively birefringent crystals are seen in association with polys (PMNs) and some crystals inside polys (phagocytized). pink cocci in pairs and chains. * Other symptoms include erythema nodosum (painful red nodules on lower extremities) and pyoderma gangrenosum (pus ulcers on lower extremities).88 - . * Staph aureus Gram stains positive. * Example would be Gram positive clusters seen on arthrocentesis. Treatment is several days of parenteral (IV) ceftriaxone. * Middle aged man with a history of gout tells you to the minute he remember when his foot became painful. * Joint fluid analysis should include WBC count. but a very hot gout joint could be 75000. But. if you do find the Gram stain or culture you have a diagnosis (so not very sensitive but very specific).Study Notes – Internal Medicine James Lamberg 28Jul2010 * Treatment should avoid NSAIDs since leukotrienes are pro-inflammatory and bad for IBD. 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. Erythema nodosum gets better with treatment of arthritis. He has no prior medical history and takes no medications. IV drug abuser. The range of motion is restricted. * Staph aureus gets into joint via direct introduction (e. Normally. * Crystal arthritis causes are gout or pseudogout. blue cocci in clusters. DO NOT DISTRIBUTE . * Another option is short-term steroids. If you do arthrocentesis the next day and the WBC count has not moved. He has noticed his ankle is red. we excrete uric acid into urine (no kidney or liver metabolism). * Most patients with a septic joint. will have negative Gram stain and cultures. infected IV catheter. Gout * 32yo man comes in with a history of right ankle swelling that occurred the night before. * Uric acid is a product of nucleic acids from cell nucleus DNA. * Neisseria gonorrhea is always hematogenous spread. Monoarticular Arthritis * Generally a single hot joint presents acutely. * Sepsis is most often caused by staphylococcus aureus infection or gonococcal infection.g. arthrocentesis. which implies the patient has had a period of bacteremia where the gonococcus is floating through the blood stream. * No matter how classic the story is. indomethacin). It can be dose-limiting when giving repeated doses. * Test every time for the first step in the work-up of monoarticular arthritis is arthrocentesis. They came to you to feel better. endocarditis. trauma from MVC or skiing accident) or hematogenous spread (e. An expected response is prompt relief of joint swelling and fever. but there are much less common. rarely vesicular or pustular) and even tenosynovitis (red streaking along the path of a tendon). All patients that have gout have a predisposition to hyperuricemia. He occasionally drinks alcohol. The problem with frequent high doses of PO colchicine is diarrhea. so give vancomycin. Patient put on nafcillin. warm. Treatment is ceftriaxone. trauma elsewhere in the body).g. * 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 not had recent trauma to his ankle. A gonococcal joint implies there has been a bacteremia. * Gonococcus Gram stains negative. the inflammatory response comes way down with NSAIDs (e. 25-50000/mL in gout/pseudo gout and > 75000 in septic usually.

and/or NSAIDs like ibuprofen or naproxen.89 - . * Since DJD is a “wear and tear” disease. Degenerative Joint Disease (DJD) * 64yo man comes to you for the evaluation of knee pain. which is the majority of patients with gout. He says he has had right knee pain for many years but recently it has gotten worse. * If patient only has gout attack a couple times a year. Another maintenance medication is colchicine. sometimes the patient may get diarrhea. which reduces the amount of uric acid in the urine. hypophosphatasia (congenital bone disease). even though it is not truly an inflammatory joint disease. Now what? Decide if he is an under secreter (give probenecid to cause more urinary excretion) or over producers (give allopurinol to reduce production). 4 Hs: hyperparathyroidism (hypercalcemia). Whatever causes the patient to have renal failure will result in under secretion of uric acid. versus RA which affects the synovium. * Treatment is the same as gout. When the neutrophils are floating around in the joint space and find a gout crystal. The disease is progressive. * Acetaminophen has no useful anti-inflammatory effect. Acetaminophen. * Probenecid is given to under excreters of uric acid to increase the excretion of uric acid. Colchicine is a good maintenance medication for recurrent episodes. they gang up on the crystals and cause inflammation. * Patient has a history of gout and hyperuricemia. so avoid probenecid in this situation. for example a manual laborer may have their hands affected. such as hips and knees. On exam you hear crepitations when he moves the joints but otherwise there is no evidence of swelling.000 range. warmth. they may be willing to suffer through some pain and take NSAIDs to relieve the attack. again nothing to do with uric acid. Pseudogout * Similar presentation as gout with arthrocentesis WBC in 25-50. * If septic joint is in the differential it is essential to do a paracentesis to ensure the joint is not septic. * Pseudogout usually occurs in patients older than 50. * DJD found in the joint cartilage. except for his left second and third DIPs. The most common cause of hyperuricemia is renal insufficiency. plus we give allopurinol to inhibit xanthine oxidase which is an enzyme important to the production of uric acid. * Pseudogout associations. Look for electrolyte abnormalities. If you see pseudogout in a younger patient. this is degenerative joint disease (DJD). Do we assume gout and treat? No. If you miss a septic joint the patient will have rapid destruction of the joint. Only about 10% are over producers. which are alcohol (uric acid is alcohol metabolite in liver) and purine foods (red meat). think about the other diagnoses (4 Hs). That is fine in DJD because this is not an inflammatory DO NOT DISTRIBUTE .Study Notes – Internal Medicine James Lamberg 28Jul2010 * Hyperuricemia occurs if you cannot excrete fast enough or you product too much. * DJD also known as osteoarthritis (OA). However. * There is no medication currently to treat the underlying degenerative process. The last thing you would want to do is put more uric acid in the urine. * Do most patients with hyperuricemia develop gout? Probably not. Then that patient could avoid daily medication with allopurinol or probenecid. * Treatment is aimed at symptom relief. hypomagnesemia. * Colchicine inhibits neutrophil chemotaxis. this is called chondrocalcinosis. it is commonly seen in older patients. aspirin. This can depend on occupation as well. Crystals are of calcium pyrophosphate. hemochromatosis (hyperpigmentation. * Disability of patients with DJD is very common. Colchicine prevents this process from happening. aspirin. He has noticed stiffness in the morning. tap the joint. Should you tap the joint every single time? Not necessarily. or erythema of the knee. * DJD is the most common form of arthritis. * Any patient with DJD who is taking over-the-counter medication should be assumed to be on acetaminophen. * Most commonly affected joints are those used the most. Notice acute gout medications (NSAIDs) have nothing to do with serum uric acid levels. They begin to develop kidney stones. You’ve treated this patient for an acute attack and he is back with more episodes. typically tumor lysis syndrome. So we have a guy with asymmetric poly arthralgia (not arthritis). diabetes). PIP joint nodes are Bouchard nodes. but that is not a very good name for the disease. * DJD most commonly occurs as an isolated condition due to overuse of joints. bone defects. * DIP joint nodes are Heberden nodes. * Say patient has four documented episodes of gout and has limited the major factors you discussed. * Say the gout patient with an inflamed ankle came back 6 months later with an inflamed knee. typically lasting less than 30 minutes in the morning. Laboratory testing is unremarkable. hemochromatosis clinical presentation. Which drug would be best for them? Answer is allopurinol. it can be seen in anyone who has extensive use of their joints such as an athlete. Predisposing factors are increasing age (more use). so we give the patients lots of hydration and diuretics if needed to flush the kidneys. He denies constitutional symptoms and other joint pain. NSAIDs are effective. * Morning stiffness in DJD is short. 90% of adult patients with hyperuricemia is due to under excretion. 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. * X-rays can show radiodense linear deposits in the articular surfaces or menisci.

Now they have a bad headache. * Treatment is steroids and often cyclophosphamide (potent immunosuppressant). * Look at urine for RBCs and protein as PAN patients can get glomerulonephritis. The pain is worse when she raises it. What diagnosis is this? This is Churg-Strauss syndrome. and loss of sensation in the right lower extremity with weakness and loss of deep tendon reflexes in that region. low grade fever for several weeks. * Typically seen in young adults or kids. Sed rates are very high. * Diagnosis is made with biopsy of the temporal artery. * Treatment is steroids. Platelet count and function are normal. * X-ray can show joint narrowing and osteophytes (bone spurs) in any joint involved including spine. This is a large vessel vasculitis. hands. Henoch-Schönlein Purpura * Patient presents with non-blanching purpura all over their body. * Can involve the kidneys with renal insufficiency. ice (not heat). * Churg-Strauss affects medium sized vessels. * It is most often seen in young women. * Treatment is steroids (e. * Treatment is steroids. * PAN is inflammation of medium-caliber blood vessels. He also complains of numbness in his foot and weakness with dorsiflexion. This is a mononeuritis (one nerve) but multiplex (motor and sensory). Wegener Granulomatosis & Goodpasture Syndrome * Patient has several episodes of hemoptysis. Takayasu Arteritis * Young woman tells you that recently she has arm pain particularly when she uses it for activity. The analgesic effect is what we want. * Takayasu arteritis affects the large vessels/branches of the aorta. with stricturing and beading (dilatation).Study Notes – Internal Medicine James Lamberg 28Jul2010 disease. * Goodpasture serology is for anti-glomerular basement membrane (anti-GBM). weight loss. a common operation. Temporal Arteritis & Polymyalgia Rheumatica * 65yo with fatigue. * The complication we worry about is sudden onset of blindness. Biopsy and serology are different. and mobilize the joints early to help prevent muscular atrophy. and now has developed hematuria. * Wegener serology can be positive ANCA (classic c-ANCA). * Biopsy of the lung or kidney will show vasculitis and granulomas. What is the diagnosis? Answer is polyarteritis nodosa (PAN). But. What is the diagnosis? Answer is Henoch-Schönlein purpura. Physical exam shows hypertension. and acetaminophen is safer in regards to renal effects and ulcers. * Treatment for painful joint should include rest. The patient complains of abdominal pain with occasional diarrhea. * Any older person with constitutional symptoms who develops a new bad headache. Goodpasture syndrome does not have upper respiratory involvement. 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. This is Takayasu arteritis. think temporal arteritis. * Serology can be positive ANCA (protoplasmic p-ANCA). * Every time Wegener is an option. Treatment can also include physical therapy. * Treatment is steroids and immunosuppressive agents if necessary. * Wegener granulomatosis affects small vessels. * Diagnosis made with angiogram. Polyarteritis Nodosa (PAN) * 45yo complains of headaches for several months and worsening abdominal pain after food. * Churg-Strauss is a profound eosinophilic picture with bronchospasm. recurrent episodes of severe sinusitis. * This is not a common disease but it is one you cannot afford to miss.g. Biopsy of purpura shows small vessel vasculitis. wheezing. * Serology can be positive ANCA (protoplasmic p-ANCA). sputum shows many eosinophils. So. You examine the arm and the pulse seems diminished compared to the other arm and femorals. There is hypertension and abdominal involvement.90 - . What is the diagnosis? Answer is Wegener granulomatosis. * Treatment can include surgical joint replacement of the knee or hip. Churg-Strauss Syndrome * Young person with non-productive cough. normal chest x-ray. * Osteoarthritis/degenerative joint disease by definition does not give a systemic inflammatory response. prednisone). Serum blood counts show eosinophil counts of 32%. place patient on high dose steroids at the time DO NOT DISTRIBUTE . showing narrowing of the take-off of various branches of the aorta. knees. diffuse mild abdominal tenderness. Sedimentation rate is very high. you will see Goodpasture syndrome as both have hematuria and hemoptysis.

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. * 47yo woman now suddenly remember she has had diabetes since she was a child and has been taking insulin for 30 years. MD -------------------------------------------------------------------------------------------------------------------------------------------Chest Pain * 47yo woman comes to your office complaining of substernal chest pain. It is intermittent and exertional. It is pain and stiffness of proximal muscles. hemarthrosis in the knee. sometimes at rest. Why not pH monitor or upper endoscopy? To rule out the most dangerous thing first. like DVT clot. better when leaning forward or worse with leaning back. with a little chest pain. pneumothorax. esophagitis. * Quadriceps biopsy of patient with polymyalgia rheumatic would not show inflammation. cancer. pulmonary embolism. PE. pericarditis. They all start with P’s. thus another prominent symptom is jaw claudication with chewing. it is not positional. What is the most common cause of atrial fibrillation in the United States? Hypertension. subarachnoid hemorrhage. if they want you to know an answer they have to tell you something. What is the most common cause of hemoptysis? Bronchitis. * What is the most common cause of non-cardiac chest pain? Gastrointestinal problems like gastritis.e. * Correcting which of the risk factors will improve her long term survival? Answer is correcting all of them. What is the most likely diagnosis? Answer is gastroesophageal reflux disease. what is the most likely diagnosis in this patient? Answer is ischemic heart disease. DO NOT DISTRIBUTE . * Polymyalgia rheumatic diagnosis is made clinical. * Which of the following is the most accurate test for her? Well then it might be pH monitor or upper endoscopy. you can have an MI with no chest pain and with a normal ECG. * Fever is not specific enough to differentiate between causes of chest pain. * Other artery branches can be involved. * Pleuritic chest pain (worse with respiration) causes include viral pleurisy (i. Conrad Fischer. * Polymyositis is associated with dermatomyositis and the presence of an internal malignancy. * Small vessel vasculitis is Wegener and Henoch-Schönlein. Now. Oh yea also most of her family members had heart attacks in the 40s and she is a high-stress type A person. Wegener. She has not past medical history. * In real life. Bornholm disease). * Any clot or collection of blood can give fever. etc. Not TB. Large vessel vasculitis is temporal arteritis and Takayasu. sometimes when she goes up two flights of stairs. Devil’s grip. no evidence of muscle inflammation (no elevated CPK or aldolase). Otherwise no one can know the answer. She also remembers hypertension and hyperlipidemia with low HDL. pleurodynia. Medium vessel vasculitis polyarteritis and ChurgStrauss. * What is the best initial diagnostic test for her? Answer is ECG. mitral stenosis. She forgot to mention she smoked three packs of cigarettes a day. Most of the time. Myocardial infarction patient complains of crushing chest pain. 4% of the time myocardial infarction pain is pleuritic. that is too small a chance so if a patient has pleuritic pain on a board exam question it is not an MI. * Smoking related deaths are about 2/3 COPD and 1/3 lung cancer. * Pneumothorax and pulmonary embolism are different from the other pleuritic chest pain in that they are associated predominantly with shortness of breath. Goodpasture. The patient is splitting and does not want to take a deep inspiration. EMG would not be abnormal. reflux disease. these things you would find in polymyositis. * Myocardial infarction chest pain changes with position 4% of the time. -------------------------------------------------------------------------------------------------------------------------------------------Kaplan Videos (2001) – Cardiology with Dr. pneumonia. peptic ulcer disease. often but not always associated with temporal arteritis. Patient complains of not being able to breath.Study Notes – Internal Medicine James Lamberg 28Jul2010 of suspicion and schedule them for a temporal artery biopsy. * Temporal arteritis is associated with polymyalgia rheumatic. * Treatment of polymyalgia rheumatic is steroids. But for a board exam. ruptured ectopic pregnancy. In real life you try to fix all of the risk factors.91 - . Chest wall is tender in costochondritis (Tietze syndrome). duodenitis. Pericarditis chest pain is positional. She also has nausea and vomiting. with a little shortness of breath. But what kind of question is that. pneumothorax (any form of atelectasis). Mnemonic is PolyMyalgia and PM for Proximal Muscles. sometimes she goes up three flights of stairs and nothing happens. For boards. Correcting which of the results in the most immediate improvement in outcome? Tobacco smoking. Always associated with a very high sed rate. MI clot. * What is the most common risk factor for coronary disease and myocardial infarction? Hypertension. * Anything that can give pleuritic pain can simulate shortness of breath. Do not wait for the biopsy results. etc. * Chest wall is non-tender in myocardial infarction. The pain has been going on for months. Fever seen in infections and inflammation like pneumonia and pleuritis as well as others like MI. subdural hemorrhage.

No need to memorize the list. They are largely based on positional changes. so diagnosis or treatment. the capillary cannot delivery the thallium. * Thallium looks like potassium to the cardiac myocyte. which is the most important: risk factors or individual presentation? Answer is individual presentation. beta blockers. Also called a chemical stress test. * Major measure of sufficient exercise (test adequacy) is heart rate. * Real exercise is always better than simulated exercise. Dipyridamole dilates coronary arteries. or best diagnostic test then pick angiogram. pleuritic. 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 not smarter than you. you want to rule out the most dangerous thing first. Dobutamine increases contractility and can provoke ischemia. tenderness on chest wall. the ischemic portion does not move well during ischemia. * Dobutamine echo stress test abnormalities found by looking for decreased wall motion. < 10% have an MI. Give aspirin (lowers mortality). Now what will you do for her? Answer is cardiac stress test. If you are a myocyte in the heart. Patient must be able to exercise. they just know what is important to listen to. not infarction). hypotension. If there is poor perfusion. What is the next best step? As a side note. You could memorize digoxin. The scan will be the same 4 hours later if there is infarct. 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. * Bicycle ergometry (hand bicycle) is not enough exercise to get the heart rate up. so more thallium should be picked up normally. * 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. If there is ischemia. 50 have a non-cardiac problem. and one leg. lightheadedness. * 47yo lady is morbidly obese. * Sub-maximal stress test should reach 85% of maximum heart rate: 85% of (220 . Profiling is less accurate. diabetic foot ulcers. shortness of breath. 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. what does this question mean? You’re being asked what is the next step in management. Thallium is injected or an echocardiogram done right after walking on treadmill. The attending knows the important symptoms that distinguish between diseases and also knows the most appropriate management. you will pick up potassium because of the sodium-potassium ATPase. For every 100 people who go to the hospital with chest pain. dobutamine echo stress test can be used when patient cannot exercise. Positional. you must have the ability to distinguish between the causes of chest pain. DO NOT DISTRIBUTE . pale. and tender. both have similar indications.age) * Exercise tolerance decreases as you get older. * 47yo lady gets an exercise stress test and it is positive. Both have similar indications. you see akinesis (no wall motion). * Maximum heart rate = 200 . cold and clammy extremities) does not help you specify between causes of chest pain. has claudication with peripheral vascular disease. Stress Testing & Coronary Artery Disease Management * 47yo lady with intermittent chest pain. calcium channel blockers (only if patient cannot tolerate beta blockers as beta blockers can decrease mortality and calcium channel blockers do not). * What if patient has baseline ST segment changes. it is not as important as presentation of positional. * Sense of impending doom and Levine sign also do not help you determine the cause of chest pain.age.92 - . * Stress echo should look for dysmotility or hypokinesis (decreased wall motion). so increased wall motion normally. * Therefore. congestive failure). tachycardia. 10 have unstable angina. just as indicated in the equation. There is much more muscle in the thighs than arms in nearly all the population. LHV. what is the best initial diagnostic test? Answer is ECG. Even with a history that includes every risk factors. Tender. * Best next step in management for patient with chest pain and ischemic heart disease seen on stress test is medication. Or. * Say the ECG is normal. No matter what happens. If you were asked next step in diagnosis then pick angiogram. the area will reperfuse showing thallium uptake. pacemaker for abnormal baseline ECG. * Reasons to stop a stress test include chest pain. just think of things that make it so you cannot exercise. doctor must be able to read ECG: look for ST segment depression (ischemia. ACE-I (if left ventricular dysmotility. dyspnea at rest due to COPD. Can she do an exercise stress test? Nope. If infracted. pain. * In terms of determining the diagnosis. nitrates (no change in mortality).Study Notes – Internal Medicine James Lamberg 28Jul2010 * Sympathetic outflow (diaphoresis. An ischemic or infracted area will have decreased thallium uptake. How do you tell the ischemia from the infarct if they both have decreased thallium uptake? You re-scan 4 hours later. pleuritic pain. Pleuritic. * Most common cause of death in the United States is myocardial infarction. * Dipyridamole thallium stress test abnormalities found by looking for decreased thallium uptake.

start diet at 100 LDL and drugs at 130. All lower triglycerides as well. risk factors or individual presentation? Again. a clot has formed and completely occluded the artery. stenting) if 1 or 2 vessel disease. Statins are first because they lower mortality. * ACE-I only helpful if CHF or decreased left ventricular function. Thrombolytics do not prevent clots from forming. Surgical mortality is 1%. ECG shows ST segment depression in V2-V4. S4 gallop. * Which raises HDL the most? Niacin. So when disease is present. lasting for the past hour. * Thrombolytics do not lower mortality either. We do not know if triglycerides are associated with disease as well as we know that LDL are related to disease. * Risk factors <=1. why do angiography? To determine if she needs a coronary artery bypass graft (CABG) or percutaneous coronary intervention (PCI) with medications. diet and exercise is not primary treatment. Only aspirin matters there. You do not hear “yea. * CABG is not done for single or double vessel disease because there is no benefit in mortality. * Heparin prevents clots from forming. give heparin. * For every 100 people who undergo CABG. aspirin. She has disease. * How can you tell now to give heparin or thrombolytics? Answer is ST elevation or not. start statin. total cholesterol. * This is unstable angina because the patient has ST depression. * 47yo woman with positive stress test and aspirin allergy. * Patient with coronary artery disease (or MI. What do you do next? Answer is statins. * Risk factors >=2. Angiography shows clean coronary arteries for Prinzmetal angina. HDL. Once you have disease. * In unstable angina. which seems small when it is someone else’s mortality. niacin. * Calcium channel blockers helpful when you cannot use beta blockers or patient has Prinzmetal angina. * 47yo woman with positive stress test but no risk factors and LDL is 171? Answer is statins. * What else should the man having a possible MI get? Nitrates. unstable angina) who has LDL > 130. Aspirin and beta blockers reduce mortality. * Nitrates and digoxin do not lower mortality. It’s better to be alive with chest pain. * If ST segment elevation present. sense of impending doom. triglycerides. it does not matter how many risk factors you have. nitrates. VLDL. a clot is forming and has not occluded the artery.Study Notes – Internal Medicine James Lamberg 28Jul2010 * What is the most accurate test for any disease? Autopsy. it does not remove the thrombus from the heart and has not been shown to significantly improve mortality. Mnemonic is MONA for morphine. or waist circumference? Answer is LDL. * PCI (angioplasty. although it is working on occluding. * Disease. * What if the patient is allergic to aspirin? Give clopidogrel or ticlopidine. short of breath. ST elevation is the best you can do to tell if there is a myocardial infarction now. do you look at LDL. * Would giving oxygen help? Not really.93 - . give thrombolytics. Better mnemonic is MONAB for morphine. although they do not lower mortality they help relieve chest pain. meaning 3 vessel disease or left main affected. 141? Statins. start diet at 160 LDL and drugs at 190 LDL. Thrombolytics is useful for myocardial infarction. nitroglycerine. not cholestyramine. * How to you differentiate Prinzmetal angina (from unstable angina)? Angiography. The pain goes to his neck and arm. he had single bypass”. He is diaphoretic. All of those drugs lower total cholesterol and all raise HDL. oxygen. not ECG. Oxygen also given as well as morphine (analgesic) but they are not the most important part. aspirin. * This is why you hear “he had triple bypass” or “she had quadruple bypass” or “David Letterman had quintuple bypass”. What is the next step in management? Give aspirin and beta blockers. If no ST segment elevation. oxygen. they lyse clots. * In a myocardial infarction. not history. Hyperlipidemia * When determining if a patient should get anti-lipid medications. angina. * What other medication lowers mortality in addition to the beta blockers and aspirin? Answer is heparin. 1 person dies. or fibric acid derivatives. CABG & PCI * 47yo woman with positive stress test. Which lowers triglycerides the most? Fibric acids like gemfibrozil. individual presentation. Let the mortality difference drive you. beta blockers. * Bypass if severe disease. * Diet and exercise only prevent the disease. start diet at 130 LDL and drugs at 160 LDL. * 47yo woman with chest pain being treated and LDL is 191. The patient is not hypoxic in the sense of low arterial PO2. get LDL < 100. Statins are first. Levine sign. * Heparin is useful for unstable angina. What is most important. Unstable Angina & Myocardial Infarction Management * 64yo man with a history of hypertension and hyperlipidemia comes to the ED with chest pain. What do you give? Clopidogrel or ticlopidine. DO NOT DISTRIBUTE . You won’t be asked diagnosis (unstable angina) or what test to order (ECG).

* Transcutaneous pacer makes the heart beat with capture. But no. Overall reduction in mortality with thrombolytics is 25%. * What about extension of the MI with cardiogenic shock? Not that either. described first in 1826 by Stokes and in 1846 by Adams near the University of Dublin. why order them? If the CK-MB is up with ST segment elevation. eptifibatide. subarachnoid hemorrhage. but troponins are even more specific (99. * All patients who get angioplasty also get a stent to keep the vessel open. * CK-MB last 1-2 days. Use tPA if patient previously got streptokinase. During times of exertion. * Cardiogenic shock would give rales. thrombolytics dissolves the clot then give heparin afterwards to keep it open. This is not the right answer though. * Think about what it could be. because streptokinase can produce antibodies resulting in anaphylaxis. thrombolytics. If they do not change management. but it also makes all the chest muscles contract. Troponin I is the most sensitive and specific. petechiae. RV infarct and cardiac tamponade could give clear lungs. but it doesn’t work that way. * Valve rupture with chordae tendineae rupture (after a week) could cause a murmur and hypotension. lasting for the past hour. you will still give aspirin. Atropine cuts the brake lines for a while. the plaque ruptures which causes a sudden clot to occlude the artery. Uterus can still make a little CK-MB but no troponins. Wait. * When a patient comes in with chest pain and ECG abnormalities. CK-MB (97-99%) is specific. LDH is not abnormal from 12-24 hours. maybe it is just not up yet since they begin to rise at 4-6 hours and take 12-24 hours to reach peak. * If valve rupture. Patient’s blood pressure is 70/40. may need to go in and emergently replace the valve. Prophylactic lidocaine suppresses those arrhythmias. so why not use lidocaine? Because it does not change the mortality. a chest that is clear to auscultation. * LDH is no longer used in the diagnosis of myocardial infarction. allowing the sympathetics to work without inhibition and thus speeds up the impulses through the AV node. has cannon a waves. Stethoscope invented shortly before by Laennec in France (1816). * Efficacy is the same with tPA (tissue plasminogen activator) and streptokinase. * If cardiac tamponade. showing complete heart block. pulse is 40. Lidocaine also causes arrhythmias. Nope. Angioplasty is when a catheter is placed through the partially occluded artery then a balloon is expanded to open the vessel. and tirofiban. The pain goes to his neck and arm. * Most common cause of death immediately post-MI is arrhythmias. You are called by the nurse because “he is confused”. We could go to sermons all day long to become saints. AV node. may need emergency bypass surgery. * What is the best initial management? Atropine. troponins last 1-2 weeks. and inferior wall. 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. * Also. * 64yo man with a history of hypertension and hyperlipidemia comes to the ED with chest pain. do a pericardiocentesis or a cardiac window then repair the hole. DO NOT DISTRIBUTE . If CK-MB not up. heavy periods. Atheromatous plaque gets covered by a little later of endothelium. but the heart would beat faster to compensate (here the patient has bradycardia). It is like a car that has an accelerator (sympathetics) and brakes (parasympathetics). Valve rupture would regurgitate into the lungs.9%). This patient has a clear lung auscultation exam. No hypotension because the blood pressure cuff did not exist then. up to a 50% reduction in mortality within the first hour. These are antiplatelet drugs and can make you bleed. * If cardiogenic shock and extension of the MI. The problem is when you remove the catheter the plaque can bulge back out. Thus you leave a meshwork stent “scaffolding” to keep it expanded. bradycardia.94 - . ECG shows ST segment depression in V2-V4. epidural hematoma. * Answer is third degree complete AV heart block. do not wait around for enzyme changes. * For MI. He received all the appropriate therapy. * Complications of an MI can all cause hypotension and hypotension can cause confusion. the management is the same for unstable angina and MI.Study Notes – Internal Medicine James Lamberg 28Jul2010 * Beside thrombolytics or heparin. Heart exam reveals 3/6 murmur. Post Myocardial Infarction Management * 65yo man in the coronary care unit (CCU) after having an inferior wall myocardial infarction last night. The mortality benefit with thrombolytics is enormous in the first 1-2 hours. a subdural hematoma. This blocks the parasympathetic. * Glycoprotein IIb/IIIa inhibitors are abciximab. 40% of inferior wall MIs also have RV infarcts. * CK-MB and troponins do not begin to arise for 4 hours. Which of the following is the most likely diagnosis? * Right coronary artery feeds the right ventricle. thrombolytics can be given up to 12 hours from the onset of chest pain (3 hours for stroke). They saw lightheadedness. beta blockers. * Myocardial wall rupture with cardiac tamponade would lead to hypotension and confusion. * Transvenous pacing cannot be setup fast enough and requires an invasive procedure. causing rales. He has melena. * What is the best initial diagnostic test? ECG. thus you would not give these in an acutely bleeding patient. cannon a waves. they didn’t have ECG back then. syncope.

bumetanide. myocardial infarction (more ischemia). and that is what a MUGA scan is about.Study Notes – Internal Medicine James Lamberg 28Jul2010 Congestive Heart Failure (CHF) * 67yo woman with a history of MI. leaky (valve regurgitation). * ABG would show hypoxia and low CO2 (hyperventilating). but they will not help acutely. and thus does not change blood pressure. morphine. * What is the most common cause of developing congestive heart failure in the United States? Post-MI. * The least accurate method to assess ejection fraction is an echocardiogram. hypertension. Dobutamine decreases the afterload. Which do you give for this patient though? Dobutamine. * MUGA scan is a nuclear ventriculogram (radionuclide ventriculography). weeks to fully take effect. But that is because your heart is not weak (cardiomyopathy). Kerley B lines. * Valvular rupture occurring a week after an MI would cause regurgitation leading to acute pulmonary edema. But you know this. You do a CXR and tell her that her lungs are filled with fluid. beri beri. * ACE-I will decrease mortality in the long-term. nitrates. Loop diuretics are furosemide. This patient has lungs filled with fluid and thus is not oxygenating. give loop diuretics. * Dopamine increases the afterload. but we know all this. 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). A CXR does not change our management in this patient. You will not be asked the diagnosis here. S3 gallop. and hemorrhoids. so you have a weak leaky heart. Common causes are stopping medications. The goal now is to decrease afterload. * Loop diuretics are used because they are intravenous and work fast on the ascending loop of Henle. like losartan or valsartan). That’s great doc. but dilate veins more. * For this 67yo patient. So you can live without the atrial kick. which is CHF in its worst form called pulmonary edema. * There are many causes of CHF and the initial diagnostic tests and management are all the same. easy. Nuclear isotope is injected into the body and the scan measures the amount of nuclear energy emitted from the heart in diastole and systole. If you have an intractable dry cough. stroke volume to be precise. * Say you give this patient oxygen and preload reduction but she is still short of breath. what is the next best step in management? Answer is oxygen then loop diuretics. dead (post-MI). it is not based on a cross sectional diameter like an echo or catheterization. But the better way is to pour fluid into the bottle and measure how much actually comes out. * Afterload reduction is best achieved with ACE-I (-pril drugs). * CXR would show enlarged heart with congestion. Most common adverse reaction to ACE-I is cough and hyperkalemia. increased salt load. but more accurate than an echocardiogram. Getting fluid out of the lungs now will help reduce preload. * There needs to be an event causing (acute) pulmonary edema in a patient with underlying CHF. Echo is the best initial method of measuring ejection fracture. it does not change management. * Patient will not die from lower extremity edema or organomegaly. Preload reduction will save this patient’s life.95 - . * Dopamine is only used if you need to raise the blood pressure. The difference in this measurement corresponds to the ejection fraction. pulmonary vascular redistribution. also known as systolic dysfunction. The fastest was to get fluid out of your body is diuretics. but not the most accurate test. Myocardial infarction killed off part of the heart. now you may have lost 40-50% of your cardiac output because you need the atrium to push blood forward. It is only used as a pressor here. * 67yo woman with CHF and now acute pulmonary edema. * ARB drugs are angiotensin II receptor blockers. valve disease. * Why not use digoxin now since it is a positive inotrope? It takes time. effusions. adriamycin use. enlarged liver. loop diuretics. torasemide. but she already knew that and she doesn’t care. enlarged spleen. Patient comes in short of breath saying they feel like they are filled up with fluid. Give her medication for her shortness of breath and to reduce preload: oxygen. * Morphine can reduce pre-load as well. Wall motion gets worse when your heart becomes ischemic. arrhythmia. This is dilated cardiomyopathy. ethacrynic acid. These patients need atrial contribution. clean. Presentation is dyspnea with rales to apices. and alcoholic cardiomyopathy. They die from pulmonary edema. edema to waist. 80-90% of patients will get better with this therapy. * Most accurate way to measure ejection fraction is MUGA scan. Since it is nuclear energy. * Nitrates also work at pre-load reduction because they dilate both arteries and veins. She comes in while chowing down on an entire pizza. * Many years ago before IV furosemide was around physicians did phlebotomy and rotating tourniquets. JVD to ears. worsening the congestive failure. * If you have congestive failure and you develop atrial fibrillation. You could look at a soda bottle and take a cross sectional diameter to get an estimate of the amount of soda inside. * How much cardiac output is based on atrial contribution? Answer is 10-20% in normal person. DO NOT DISTRIBUTE . give an ARB (-sartan drugs. radiation to her heart and chest. Chagas disease. * Dopamine and dobutamine are both positive inotropes. * Catheterization and angiogram is less accurate. They are cheap. What are you going to do to help her is the question. They will both increase contractility (positive inotropes) and myocardial oxygen consumption.

Mnemonic: SAD for syncope. 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. you need an underwear transplant. slicing a piece of the dilated heart out. * The ease of availability and use of the echocardiogram has led to a decline in our ability to auscultate murmurs. but not a regurgitant loose/floppy lesion. atrial fibrillation (with emboli to brain). it will be too late. * These exotic findings are usually only seen in longstanding non-treated disease. There can also be hoarseness as the atrium presses against the recurrently laryngeal nerve. heart transplant needed.g. None of these have utility in making a diagnosis. * What is the most common cause of mitral stenosis? Rheumatic fever. HLA-B27 stuff. angina prognosis is 5 years. coronary artery disease is common in patients with aortic stenosis (older men). like Watson water hammer pulse. Becker sign. furosemide. edema). but not stenotic lesions. * Calcification can cause mitral stenosis and aortic stenosis. We replace the valve before these patients join the American Iatrogenic Association. and angina. * Infections (e. * Rare aortic regurgitation causes include ankylosing spondylitis. dyspnea (CHF). Sometimes you may need digoxin.Study Notes – Internal Medicine James Lamberg 28Jul2010 * 67yo lady with pulmonary edema and CHF was treated with oxygen. Rosenbach sign. they increase ejection fraction and cardiac output. Going back to stress testing. Hearing a diastolic murmur is more reliable. The actin and myosin filaments have become separated and cannot contract well. Ehlers-Danlos. Valvular Heart Disease * Valvular disease is organized into stenosis and regurgitation. Batista partial ventriculectomy). * Since nothing can be done after the heart dilates. but it can cause any valvular disease. reactive arthritis. Infarction can cause regurgitant lesions through this mechanism. and dysphagia. Don’t forget the even less common Lighthouse sign. endocarditis) can cause regurgitant lesions from vegetations. * Aspirin has been shown to decrease mortality in coronary disease but not congestive failure. the weak heart or the ischemia? Ischemia. You give potassium if the patient is only on diuretics and digoxin.96 - . but it can cause any valvular disease. 1-2 years average until death.g. * What else causes mitral stenosis? Congenital. DO NOT DISTRIBUTE . The echo has greater sensitivity and specificity than the stethoscope. Quincke sign (pulsation of the capillary bed in the nail). and that is why beta blockers are good as they lower heart rate and cardiac contractility. what is the major determinant of exercise? Heart rate. Mayen sign. do you cut out a piece of underwear to fix the size? No. * Diuretics and digoxin have not been show to lower mortality. syphilis. because the ostia (entry points) for the coronary arteries are distal to the aortic valve. S3 gallop. if you plan to replace the valve you should not wait for the heart to dilate up in size. Müller sign. * What is the bigger problem in cardiac failure with systolic dysfunction. Traube sign (a double sound heard over the femoral artery when it is compressed distally). Corrigan pulse (rapid upstroke and collapse of the carotid artery pulse). ACE-I has been shown to improve mortality. Lincoln sign. Worse prognosis is with CHF. If you wait. CHF. morphine. Most common symptom of aortic stenosis is angina. Sherman sign. * But won’t beta blockers worsen ejection fraction? Actually. She feels all better the next day. because they are antiischemic. * Mitral stenosis is the most likely valvular disease to have hemoptysis. Gerhardt sign. When you lower the heart rate you reduce ischemia and the patient is less likely to die. Syncope prognosis is 3 years. Anything that dilates the heart has to cause regurgitation because the leaflets separate. * Aortic stenosis is associated with syncope. and Ashrafian sign. and beta blockers. Dysphagia because the enlarged left atrium (most posterior heart structure) presses on the esophagus. * When your heart dilates. * What can be done to restore a heart to normal shape and size once it dilates? Nothing. * ACE-I can raise potassium and help offset diuretics. the valve leaflets do not change in size. does not work (e. * Fundamental symptom of all valve disease is CHF (rales. Also. The stenotic aortic valve blocks blood flow into the coronary arteries. Landolfi sign. Duroziez sign (systolic and diastolic murmurs described as 'pistol shots' heard over the femoral artery when it is gradually compressed). That thing is that they do not die. nitrates. 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. Cardiomyoplasty. Marfan syndrome. but they do not alter anatomical heart size. angina. * ACE-I may stop the dilation problem from getting worse. * There is an interesting thing that happens to patients with congestive failure who are on beta blockers and they like it quite a bit. * Beta blockers lower mortality more than ACE-I in congestive failure. more than by valve location. thus another cause of angina. * Exotic findings for aortic regurgitation are largely archaic. as the diuretic would make you hypokalemic and the digoxin would then become toxic. what is the most important medication to discharge her on? Answer is ACE-I. de Musset sign (head nodding in time with the heart beat). Hill sign. diuretics. When your butt gets really big and your underwear stretches. That was because beta blockers had not been studied in congestive failure because everyone thought it would make things worse.

* Aortic stenosis (AS): crescendo-decrescendo murmur. If the porcine valve needs to be replaced every 10 years and we have a 27yo pregnant female here. pansystolic or holosystolic murmur. This makes it easier for blood to get out of the heart. Do not give HOCM or MVP patients diuretics. and afterload 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. so anything that makes the heart larger (more blood) pushes away the obstruction and decreases the murmur. * Mitral regurgitation (MR): S1 and S2 are obscured by constant murmur. She delivers here baby but still has bad shortness of breath despite diuretics and salt restriction. aortic at upper right sternal border. * 27yo pregnant woman with much worse symptoms from her mitral stenosis. * Aortic stenosis calcifications are from calcium. AR. Valsalva). * Commissurotomy would help increase the size of the stenotic hole. 5mmHg laying flat. and we do not have a problem with that in mitral stenosis. mitral at lower left midclavicular area. Digoxin would help with atrial fibrillation because it helps decrease the heart rate and ventricle fills during diastole. the heart contracts more completely causing more obstruction. * With aortic stenosis. lower left heart apex. Cardiac Auscultation * Auscultation locations are APTM (“all physicians take money”). panic attacks. positive inotrope. and ACE-I would thus cause more obstruction. Treatment is preload reduction. Why? Plasma volume goes up but the size of the mitral valve does not. is valve replacement at the top of your list for management? Lets hope not. Asymmetric septal hypertrophy is in the way. and MR. * Hypertrophic obstructive cardiomyopathy (HOCM): crescendo-decrescendo murmur. * Cardiac catheterization is the only way to get direct pressure readings for any valvular disease. blood basically just falls into the right atrium. thus balloons do not work as well. * Valsalva maneuver decreases preload. Palpitations. * Do not give beta blockers to AS. What is the next best step in the management of this patient? Balloon valvotomy. If you increase the intrathoracic space pressure (valsalva) it pushes blood out of the thorax. Blood is brought away from the legs and into the heart. Most common presentation is dyspnea. upper right sternal border. * Leg raising increases preload. blood pools in the legs so less blood in the heart. * The ultimate step in management for all valvular heart disease is replacement of the valve. tricuspid at lower left sternal border. It is the most common cause of sudden death in healthy young athletes. Digoxin will not help because it helps blood squeeze out of the ventricle. MS. * Transthoracic echo (TTE) or transesophageal echo (TEE) first? Answer is TTE first. salt restriction). Digoxin. But this is very invasive. * Right atrial pressure when sitting is zero. When dehydrates. palpitations. the heart empties more fully causing more obstruction. when standing it could be almost sub-atmospheric. Best initial therapy for HOCM is beta blockers because it decrease the heart rate thus more filling and thus less obstruction.Study Notes – Internal Medicine James Lamberg 28Jul2010 * Initial test of choice for any valvular disease is echocardiogram. which increases intrathoracic pressure and decreases venous return to the heart. Decreases with preload reduction (standing. ACE-I and vasodilators are the most important. * Mitral stenosis treatment includes preload reduction (diuretics. * With balloon valvotomy a vascular catheter is threaded across the valve and a balloon dilates. Decreases with preload reduction (standing. that is the question. * Squatting maneuver increases preload. then you hear the blood crashing down on the ventricle. But what can you do in the meantime before replacing the valve.97 - . MR because it would make the murmur/problem worse. Most common cause is congenital. Initial therapy is beta blockers. Valsalva). AR. Valsalva). Treatment is valve replacement if symptoms persist. Have patient bear down like they are having a bowel movement is another way. * Mitral regurgitation and aortic regurgitation are managed with the same medications used for CHF. MS. When a patient exercises. Valsalva). balloon valvotomy does not work well. * Note treatment and maneuvers are the opposite in HOCM and MVP compared with AS. * Mitral valve prolapse (MVP): mid-systolic click due to leaflets stopping short. * Standing suddenly decreases preload. Murmur will increase with more blood in heart (leg raise. there is more murmur with less blood and less murmur with more blood. Valve replacement with vessel bypass is the therapy. diuretics. Pain. Murmur will increase with more blood in heart (leg raise. Panic attacks. Decreases with preload reduction (standing. Mnemonic: Prolapse. Presentation is most commonly pain (atypical chest pain). opening the valve. Unlike the other murmurs of the left heart. squatting). DO NOT DISTRIBUTE . * ACE-I help get blood out of the ventricle. * Occasionally a myomectomy is needed for HOCM to remove the obstruction. Exhalation against closed glottis. Leg veins are compressed pushing blood up into the heart. squatting). Which is best? TEE. Decreases with preload reduction (standing. * Aortic regurgitation (AR): decrescendo murmur because blood gets shot up out of the aortic valve and you do not hear anything. pulmonic at upper left sternal border. How do you get the valve into the heart? Open heart surgery in general with median sternotomy. There is no pressure pushing blood back into the heart.

Study Notes – Internal Medicine James Lamberg 28Jul2010 * If a diuretic is used to treat a murmur (preload reduction). * First test of choice is echocardiogram. * Sinus bradycardia at a rate of 47 in an asymptomatic man.. * Causes of pericardial tamponade are pneumonia. * Which connective tissue disorders have pulmonary involvement? Any connective tissue disorder. standing). * Causes of restrictive cardiomyopathy include amyloidosis (protein accumulation from inflammatory disease). inflammatory.. rickettsia. Arrhythmia Management * The type of arrhythmia management that you need to know is the first hour of management. What if the heart rate was 37 without symptoms and ECG showing sinus bradycardia? Do nothing. DO NOT DISTRIBUTE . scleroderma. But that could be pulmonary edema. viral (e. * Treatment is to remove the pericardium. * 47yo man comes to the office seeking advice about diarrhea prophylaxis prior to going to a vacation to Thailand. while the medical students will look at each other and say “Uhh. Gram negatives. Restrictive Cardiomyopathy. uremia. yep anything. rheumatic fever. klebsiella. * The problem with the pericardiocentesis is that the fluid can keep re-accumulating. staph. If NSAIDs do not work. * Inflammatory causes include SLE. * Presentation is jugular venous distension (JVD). If no etiology (mainly viral). toxoplasmosis. Heart rate is seen on ECG. What are you going to learn from this? Pretty much nothing. cytomegalovirus. mediastinal lymph nodes are all near the heart. pneumococcus most often. trauma. same causes there too. pulse rate is not the same as heart rate. What is the next best step in management? This patient does not have symptoms so ECG. anaerobes. Dressler syndrome. * Causes of pericardial tamponade are the same as pericarditis. Viral is the most common. breast. pseudomonas. what you would be expected to managed as a physician intern at a hospital.yea no point. ascites. * Treatment of pericarditis is to correct the underlying etiology. * Trauma causes include open heart pericardiotomy trauma. * Chronic pericardial tamponade becomes constrictive pericarditis from fibrosis. cancer. Infections. hemochromatosis. 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. tachycardia. then a Valsalva will make the murmur less intense by the same concept of preload reduction. * Cancer causes include. ACE-I and diuretics are not used because it is not dilated. Lungs.g. it’s any cancer near the heart. * Can trauma cause a pleural effusion? Yep. two hours post prandial in the supine position. cancer. and fibrosis. & Pericardial Tamponade * Beta blockers are not used in restrictive cardiomyopathy because it is not hypertrophic. * CXR or CT for diagnosis. * What are the causes of pneumonia? Anything. squatting) and less intense with less blood (Valsalva. enlarged liver. Exceptions are HOCM and MVP. syphilis. * Treatment of choice is needle pericardiocentesis. give atropine acutely to increase the heart rate then a pacemaker later on. All the attendings and residents who know the lists will love the ever so complete lecture. next step is leave him alone. Pericarditis. * Normal heart rate of 60 to 100 is based on thousands of military recruits between the ages of 18 and 24. * Symptom of pericarditis is pain that is positional and pleuritic. Pericardial knock. pleuritis. so how do you distinguish? Answer is pulsus paradoxus and clear lungs. NSAIDs. chest wall trauma. Sjögren syndrome. Any major textbook will list these items in completeness. You notice that he feels alright but his heart rate of 47. If he did have symptoms. pulse is palpated. * Say you’re in a lecture and someone is listing all the causes of pericarditis. * What occurs in constrictive pericarditis that does not occur in CHF. * What about peritonitis? Yep. but you can bundle any one of the causes into these main topics. * ECG shows ST elevations everywhere. and hypotension. a hole in the pericardium and fluid drips into pleural space. * Causes of pericarditis include tuberculosis. * Side note. It does not matter how low it gets because he has no symptoms. yep stop cause it’s any trauma.98 - . esophagus. coxsackie). then use prednisone. * What cancer can affect the lung? The ones that are anatomically near the lung. Thus all left sided murmurs get more intense with more blood (leg raise. wanna go get a beer?” * There are over 50 separate causes of pericarditis. rheumatoid arthritis. strep. Pathognomonic ECG finding is PR segment depression. yep any connective tissue disorder or inflammatory disorder. pleural effusion. Try to do this for any disease with a long list. sarcoidosis. And pulmonary contusion with atelectasis leading to pneumonia. So what do you do to treat a chronic pericardial effusion? Pericardial window. * Constrictive pericarditis symptoms are JVD. mixed connective tissue disorder.

He is found to have ventricular tachycardia (Vtach). Call for help before moving on to the rest of the algorithm. becomes lightheaded and confused. * 72yo former president of the U. circumferential digital rectal examination. and get the tube in. * After calling for help. We do not wait for the patient to have their first syncopal episode while they are driving down the road. * Mnemonic for SVT meds: ABCD. check pulse. adenosine. Determine if the patient is responsive and not just sleeping. * Vtach that is stable gets lidocaine. pulseless electrical activity (PEA). * Mobitz type II AV block is the dividing line. he has no pulse so we start compressions. You can give digoxin. Now what? Defibrillation. he has lightheadedness and confusion. What’s the problem now? Well. beta blocker. or confusion. falls to the floor and is not moving. The indications for digoxin. Open airway. DO NOT DISTRIBUTE . is at an important dinner in Japan. We have to agree on a definition for hemodynamic instability. * Coumadin is used when patient has chronic atrial fibrillation. atrial fibrillation (Afib). start compressions if no pulse. this can progress to complete block and ischemia. they keep you alive while waiting for the important equipment (defibrillator) to arrive.Study Notes – Internal Medicine James Lamberg 28Jul2010 * First degree AV block without symptoms do nothing. He is found to have rapid atrial fibrillation secondary to Graves disease. alcohol. * Say patient is truly unresponsive to even painful stimuli. This does not progress to second degree AV block. do synchronized cardioversion. * Say patient had a history of asthma? Then do not use beta blockers because it could cause bronchospasm. no one is coming to bring a defibrillator or take this man to the hospital. SVT) first step is vagal maneuvers like carotid sinus massage. calcium channel blocker. What does unstable mean though? Hemodynamic instability means systolic blood pressure < 90. shortness of breath. She comes in complaining of palpitations. calcium channel blocker. What is the next step in management? Call 911. * 28yo female medical student who has been preparing for an exam and using the four basic food groups. * Mobitz type I AV block (Wenckebach) without symptoms do nothing. mammalian dive reflex (mostly for kids.g.. then slow the rate. Chest compressions do not restart the heart. beta blocker. leans forward and vomits all over the Japanese ambassador. gets up to make a point. calcium channel blocker. * Rate controlling meds for non-SVT atrial arrhythmias are BCD: beta blocker. * 57yo man at the opera who gets up. and beta blocker in this scenario are the same so it does not matter. * Say ECG shows up and patient is in Vfib with no respirations. * Stable patient with SVT and vagal maneuvers did not work. suction.S. Valsalva maneuver. ECG shows supraventricular tachycardia (SVT) at a rate of 160. * Determine if the patient is unstable. you better be sure about the next step of management. * Conduction jelly is used to increase the surface area for the shock and to decrease the burn because dry skin burns. Because after you have had Afib for more than two days you are at risk for emboli. * Stable patient atrial arrhythmia (e. If unstable. * Mobitz type II AV block and type III complete AV block get a pacemaker even without symptoms. They are all the same in their management except adenosine. 40% of your patients just died since 10% are lost per minutes. This does not usually progress and is part of the normal aging of the conduction system. then adenosine. What is the only way to distinguish these? ECG. * If vagal maneuvers and adenosine do not work. Thus. the patient has no good chance of survival. you better call for help to get the equipment there so you can distinguish these. chest pain. unstable gets defibrillation. * 57yo man at the opera who gets up. What is the next best step in the management of this patient? * Does he have hemodynamic instability? No. then you do ABCs.. In that time. so don’t do that. American Heart Association has spent a great deal of time working the algorithm out. how long would it take to intubate in the field? Maybe 3-4 minutes with getting equipment out. Adenosine only used for SVT. calcium channel blocker. * Say the patient is unresponsive and pulseless. ventricular fibrillation (Vfib). check breathing. caffeine. * Eyeball pressure does a good job of slowing the heart rate. What is the first step in management? * Multifocal atrial tachycardia includes SVT. ice back to face). * Survival without defibrillation declines to zero after ten minutes. give two breaths if not breathing. * Does that mean a person with a normal systolic blood pressure of 88 gets shocked in this situation? Yes. Thus. atrial flutter (Aflutter). Eyeball massage can cause retinal detachment and it is not needed. digoxin. After ten minutes without defibrillation. asystole. What is the next best step in the management of this patient? If stable.99 - . Say we skip this step and open the airway. How do you know which one to use? These all slow the rate but do not convert the rhythm. Not intubation. do a couple of rescue breaths. What is the differential? Pulseless ventricular tachycardia. There is a 10% decline in mortality per minute. What is the next best step in the management of this patient? Answer is determine if he is conscious or unconscious. Blood pressure is 128/88.and blinding the patient. beta blockers because it will block the effect of the sympathetic outflow from the hyperthyroidism. or digoxin. nicotine. which means > 48 hours. chocolate.

not uncommon. * ECG shows Vfib and you’ve gone through cycles of CPR with defibrillation. The amount of energy needed for successful defibrillation is little at the very beginning. 10-20J of energy. Thus. etc. What medication can you give for refractory VT or VF? Amiodarone. atropine and epinephrine can be given between CPR cycles. the patient is dead anyway. You consider pacemaker because it could possibly be very slow bradycardia and you may have missed a beat. * Ectopic beats originate from an ectopic focus. * Supraventricular can be differentiated from ventricular by the width of the QRS complexes. * What if ECG shows Vtach and patient is unconscious? Defibrillation. The patient states DO NOT DISTRIBUTE . * For asystole or PEA. so it might not be perfectly flat line. * Resuscitation of patients beyond 10 minutes only in hypothermia or induced hypothermia. * Intracardiac medication has not been show to have greater efficacy so it is not an answer. Each large box is 200ms. Don’t think something like the leads came off the patient’s chest. it’s more like rebooting an electronic device when it is not functioning well. then epi and atropine for a few rounds. After three cycles with refractory VT or Vfib. * What about the dosing of these drugs and shocks? Drug dosing is not asked on board exams. You feel a pulse and note that it is 70 per minute. You can differentiate tachycardia from bradycardia this way. * Magnesium is given for Torsades de Pointes only. * PR interval should be less than 5 small boxes (200ms). do a cycle of CPR then shock again. * Consistent wide complexes is ventricular tachycardia. So shock. Defibrillation stops the heart with the hope that it will reboot normally. use that instead. there is nothing else to do. drug. atropine is 1mg for cardiac arrest and 0. * Important Note: There is no minimum and no maximum for running a resuscitation. 50. any arrhythmia. * You are at the bedside for a patient with chest pain. * Say you’ve given epinephrine and atropine through several cycles of CPR and the patient is still dead. * Arrhythmia associated with digoxin toxicity is bigeminy.Study Notes – Internal Medicine James Lamberg 28Jul2010 * If defibrillation did not work. Irregular waves with no consistency across the rhythm strip. Count the number of large boxes between QRS complexes and divide 300 by that number. lidocaine is 1mg/kg. If you have a defibrillator. The most common arrhythmia seen in digoxin toxicity is SVT with variable block. For true asystole. * Each small box is 40ms. Exception may be the advanced cardiac life support (ACLS) drugs here. QRS should be less than 3 small boxes (120ms). Electrocardiograms * There are very few ECGs on USMLE Step 2. Side note: always confirm asystole in a second lead. What do you do next if the patient is conscious and stable? Give lidocaine. then consider a pacemaker. 60. shock. this does nothing. * Know what ventricular fibrillation looks like and do not expect Torsades. You can consider a pacemaker. * Do not shock asystole. CO2 production of each cell and oxygen consumption is directly proportional to body temperature.5mg for bradycardia. 150. * You get called into a room by a nurse because the monitor shows the patient’s rate at 140 per minute. Two is couplet. How much time do you have to save this patient? 10 minutes. What do you do? Defibrillate. * 300 method points are 300. you can give amiodarone or lidocaine. There is some biological variability. Epinephrine is 1mg. * Precordial thump is like a little defibrillation. Now you intubated the patient and give epinephrine during the cycles. One is PVC. They become unconscious and the ECG shows flat line. * Thoracotomy with direct cardiac massage is also not an answer. trigeminy. * Counting rate is done by the 300 method. adenosine is 6mg to start. it will not help. Patient is always pulseless. Supraventricular impulses follow the normal conduction pathway through the AV node. This is asystole. Three is triplet. maybe two or three. Defibrillating asystole will do nothing because the electrical system is already stopped. which makes them narrow on the QRS. amiodarone is 300mg.100 - . Wide complexes are > 120ms. 75. CPR. Couplets are two PVCs. Should you do a precordial thump for the witnessed arrest? No. precordial thump used in witness arrest only with no defibrillator present. Four or more is ventricular tachycardia. Precordial thump is like defibrillation and you do not defibrillate flat line. drug. * Bigeminy is every other beat being a PVC. So if there were 5 large boxes between QRS complexes it would be 300/5 = 60bpm. CPR. Epinephrine can be given between each cycle as well. She has the defibrillator ready and is asking you what to do. it’s not like jumper cables for a car. Wide complexes always comes from the ventricles. * ECG showing flat line. 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. Algorithm says consider because beyond that you are considering burial or cremation. then consider the patient dead. What is the best next step in management? CPR. 100.

-------------------------------------------------------------------------------------------------------------------------------------------- DO NOT DISTRIBUTE . * When talking about peaked T-waves. The pointier the worse.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.101 - . * The most important ECG to know is regular sinus rhythm. The peaked T-waves are so high that the monitor is reading them as QRS complexes. the size does not matter as much as the shape. 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.

Sign up to vote on this title
UsefulNot useful