Study Notes – Internal Medicine

James Lamberg


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: -------------------------------------------------------------------------------------------------------------------------------------------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.



Study Notes – Internal Medicine

James Lamberg


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



Study Notes – Internal Medicine

James Lamberg


* 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.



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

37) In a diabetic patient with proteinuria. whereas anemia of chronic disease is marked by an unusually low TIBC. look at the hand veins. 24) Three liters of Coca-Cola administered via nasogastric lavage over a 12-hour period can dissolve gastric bezoars. esophagus. but the problem is less frequent and smaller in magnitude with ARBs because of their less pronounced effects on aldosterone levels. cervix. the minimum amount of free air that can be detected on an upright chest x-ray is 12mL. It is thought that the cola acidifies the gastric contents and liberates carbon dioxide in the stomach. 29) The three major openings in the diaphragm through which hernias may occur are the esophageal hiatus (most common). resulting in a shortened 22 or Philadelphia chromosome (Ph1). 44) Bartter's syndrome is a disorder associated with normotensive hyperaldosteronism. 43) Ethylne glycol (antifreeze) toxicity is characterized by high anion gap metabolic acidosis. 50) The cytogenetic marker of chronic myelogenous leukemia is the 9:22 translocation. 42) D-lactic acidosis is characterized by increased serum anion gap. look for a squamous cell cancer (lung. Because up to 50% of patients develop gallbladder carcinoma. the chance of developing breast cancer can be reduced by about 50% with the use of tamoxifen. look for vocal cord paralysis. 49) The triad of thrombocytopenia. 39) In resistant hypertension. in which portions of the long arms of chromosomes 9 and 22 are exchanged. 41) The principal mechanism of bicarbonate reabsorption in the proximal tubule is through Na+-H+ exchanger (NHE3) activity. perform a biopsy. anus). If the patient has a clinically suspicious lump. a sign of mediastinal involvement (recurrent laryngeal nerve) that renders the patient inoperable. usually left-sided). fragmentation hemolysis. and severe renal potassium wasting. consider and rule out renovascular hypertension. 25) Regardless of what is done. 36) The presence of bilateral small kidneys in a patient with azotemia confirms chronic renal failure. GI bleeding stops spontaneously in about 80% of patients. prophylactic cholecystectomy is recommended. 46) Hypochromic microcytic anemias are the most encountered anemias in hospitalized and ambulatory patients. 38) Treatment of anemia of chronic renal failure by recombinant human erythropoietin is highly effective. lung. there is a high chance of superior vena cava obstruction. hypokalemic metabolic alkalosis. periodic vaso-occlusive disease ("crises"). 35) Up to 15% of breast cancers may not be detectable by mammogram. 33) Patients with head and neck cancer have a 30% chance of developing another cancer somewhere in the aerodigestive tract (head and neck. 27) About 90% of patients with primary sclerosing cholangitis have underlying ulcerative colitis. 47) Both iron-deficiency anemia and anemia of chronic disease have a low transferrin saturation. and often by itself effective therapy. 30) In a patient who has a malignancy involving the right hilum. head and neck. but less than 10% of all patients with ulcerative colitis have primary sclerosing cholangitis. In iron-deficiency anemia. 40) New onset of nephrotic proteinuria in an elderly patient warrants exclusion of an underlying malignancy. 26) Patients with hereditary nonpolyposis colorectal cancer syndrome have a higher-than-average risk of developing colon and gastric cancer. perhaps the most spectacular of the fragmentation syndromes. If the veins in the hands are distended and do not collapse when the arms are lifted over the head. chronic end-organ damage. and fluctuating neurologic signs suggests thrombotic thrombocytopenic purpura (TTP). 31) In high-risk patients. 48) The main clinical manifestations of sickle hemoglobinopathies are hemolytic anemia. but correction of iron deficiency and iron supplementation by oral or intravenous route is simpler. DO NOT DISTRIBUTE -5- . and foramen of Morgagni (rare). or esophagus). secondary to juxtaglomerular hyperplasia. foramen of Bochdalex (3-5%. 28) In patients with suspected perforation. metabolic acidosis. especially in younger (< 20 yr) or older (> 70 yr) patients. neurotoxicity in the form of ataxia. Some patients with acute lymphoblastic leukemia (ALL) also have 9:22 translocations (poor prognostic marker). and hyposplenism. especially if they continue to smoke and drink. and calcium oxalate crystals in the urine. more common in women who have gallstones. seizures. and episodic encephalopathy in patients with short bowel syndrome. the presence of concomitant retinal disease suggests strongly (90% correlation) that the renal manifestations are due to diabetes. 34) If a patient presents with hypercalcemia. 45) Hyperkalemia is an important side effect of both ACE inhibitors and ARBs. 32) If a patient with lung cancer presents with hoarseness.Study Notes – Internal Medicine James Lamberg 28Jul2010 23) Porcelain gallbladder is an incidental finding. the TIBC is often increased. cheaper. resulting in the disintegration of phytobezoars.

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

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

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

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

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

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

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

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

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

Study Notes – Internal Medicine

James Lamberg


* The best (most accurate, most sensitive) test for the diagnosis is electromyography (EEG) looking for a decrease in the action potential spike on repetitive stimulation. * MG is essentially an autoimmune disease against the acetylcholine receptor. * Treatment is symptomatic for weakness and for the disease with autoimmune suppression. * Symptomatic treatment is with anticholinesterase medication (neostigmine, pyridostigmine) to raise the level of acetylcholine in the synapse, improving the weakness. * To treat the autoimmune disease, give prednisone, azathioprine, IV immunoglobulin, plasmapheresis, and thymectomy. Prednisone is best initial immunosuppressive because it takes 1-3 months to have an effect. Patients may initially have a worsening of their disease. Azathioprine takes 3-6 months to have an effect. * If acute myasthenic crisis, use IVIg or plasmapheresis to improve the patient’s crisis immediately and acutely. * In patients with GBS or MG, you must follow their respiratory status. The diaphragm is a skeletal muscle and when the disease involves the diaphragm the patient can go into respiratory failure. So, always consider the possibility of an intubation and respiratory support to get them through the crisis. -------------------------------------------------------------------------------------------------------------------------------------------Kaplan Videos (2001) – Pulmonology with Dr. Asher Kornbluth, MD -------------------------------------------------------------------------------------------------------------------------------------------Read the last line of the question stem to help determine what organ system the question is asking about. This will help you develop a better differential diagnosis as you read the question. -------------------------------------------------------------------------------------------------------------------------------------------Pulmonary Function Tests * A pulmonary function tests (PFT) is generally used to differentiate between obstructive and restrictive disease. There may be a great deal of overlap between these. * Tidal volume is normal in-and-out respiration at rest. Good rule of thumb is 10mL/kg, so 700mL for a 70kg patient. Vital capacity is deep breath then exhaling maximally, does not empty lungs completely. Residual volume is left over lung volume after vital capacity. Vital capacity plus residual volume is total lung capacity. Residual volume is a difficult measurement to make and not done in clinical practice, so you never know the exact total lung capacity. * In restrictive pattern, all lung volumes are decreased. Therefore total lung capacity is decreased. Lungs are restricted and cannot expand due to disease such as sarcoidosis, interstitial fibrosis, and chronic tuberculosis. * In obstructive pattern, there is an obstruction in getting air out of the lungs; a hallmark of asthma and chronic obstructive pulmonary disease (COPD). Residual volume will be higher because you cannot expel all of it. Over years, the total lung capacity will increase with increased residual volume. This is what causes the large AP diameter, giving the barrel chest appearance. Measures of air outflow are reduced in obstructive disease. * FEV1 measured by having patient take deep breath in then breath out as fast as possible, with the forced expiratory volume measured over 1 second. * FVC is the forced vital capacity, basically the same as vital capacity. * FEV1/FVC ratio is decreased in obstructive disease, mostly because FEV1 is low. So FEV1 and FEV1/FVC low. * FEV1/FVC ratio is normal in restrictive disease, with low FEV1 and low FVC. * FV25-75 is forced volume between 25% and 75% during a vital capacity. FV25-75 reduced in obstructive. * Residual volume high in obstructive lung disease, low in restrictive lung disease, but RV not easy to measure. -------------------------------------------------------------------------------------------------------------------------------------------Alveolar-Capillary Membrane Diffusion * Diffusion capacity is a measure of alveolar capillary membrane, not an easy measurement to do. Alveolarcapillary membrane gets destroyed/fibrosed in emphysema. If the DLCO (diffusion of the lung carbon monoxide) is low, implies destruction of the alveolar-capillary membrane, so emphysema or ARDS (acute respiratory distress syndrome). ARDS patients are generally in the ICU on a respiratory so a DLCO isn’t measure. * In bronchitis DLCO may be normal, in emphysema DLCO may be low. * Simpler way to measure gas exchange effectiveness is by measuring alveolar-arterial difference in oxygen, the AaDO2 or Aa gradient. This involves getting an arterial blood gas (ABG) after performing an Allen test to ensure ulnar collateral circulation (not sensitive but still done). On ABG, lab gives you pH, PCO2, PO2. * Say PO2 80mmHg (normally 90-100). Alveolar O2 at room air (21% O2) is 150 - 1.2*PCO2. * Normal PCO2 is 40, so Alveolar O2 would be 150 - 1.2*(40) = 102. Difference is achieved by subtracting what O2 you got in the blood gas (80mmHg), so 22 here. This is mildly elevated as normal is 5-15. * If there is a pulmonary process affecting the membrane, A-a gradient may be as high as 40. * Say our ABG comes back as 7.4/20/100. Alveolar is 150-1.2*20 = 126. 126-100 (PO2) gives 26 for Aa gradient. * Think about this physiologic process. The patient is breathing very fast to get PCO2 down to 20, so you know there is some problem. That is why measurement of PO2 does not tell you what kind of gas exchange you have.


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Study Notes – Internal Medicine

James Lamberg


* So in summary, A-a gradient tells you what is going on for gas exchange at the alveolar-capillary membrane. * Given 7.4/36/96. Find Aa gradient. 150-1.2*36=107. 107-96 is 11 for Aa gradient (normal range). -------------------------------------------------------------------------------------------------------------------------------------------Solitary Pulmonary Nodule * A solitary pulmonary nodule is a single nodule less than 6cm. Lung cancer is rarely cured. The only time you can cure is if you have a solitary cancer and resect before it metastasizes. * So you found a < 6cm nodule on chest x-ray. What are the criteria for just following this nodule? Young patient (<50yo) and non-smoker. If this is the case, repeat the chest x-ray every 6 months for 2 years. If the nodule has not changed size, we know it is benign. Tell patient to take CXR with them next time they go for an x-ray. * If you are looking for calcification within a nodule, do a chest CT scan due to increased sensitivity. * Popcorn appearance (scattered areas) of calcification within nodule, think hamartoma (e.g. hair, tooth). * Central or bull’s-eye calcification within nodule, think granulomatous disease (e.g. tuberculosis). * Eccentric (near edge) single area of calcification within nodule, think possible malignancy. * Say patient is 60yo and 50pack*year smoker. You find a 2cm nodule on CXR. Next step is do a biopsy, most of the time by open lung biopsy. Usually nodule is not central enough to reach with simple bronchoscopy. If the biopsy shows malignant cells, next step is surgery to remove. If benign, follow with CXRs. -------------------------------------------------------------------------------------------------------------------------------------------Pleural Effusion * The pleura covering the organ (the viscera) is the visceral pleura. The pleura outside that is the parietal pleura, with fluid between the two pleurae. When fluid increases between these two, this is a sign of a pleural effusion. * Early sign of pleural effusion is loss of costophrenic angle at the diaphragm, requires about 300mL of fluid. * Lay patient on the side of the effusion and do a lateral decubitus x-ray. If the effusion is free-flowing, the fluid will layer out into the dependent portion. This is useful to know to determine if you will get fluid via thoracentesis. If the fluid were trapped, we have to hit the trapped portion itself. * Pleural effusions classified into transudate and exudate. In general, exudate is seen in sicker patients. Transudate is seen in high-pressure differences (e.g. CHF) or low blood oncotic pressure (e.g. nephrotic syndrome, cirrhosis). Cirrhosis causes hypoalbuminemia (protein not created) typically resulting in right pleural effusion. * To differentiate, need pleural LDH and protein, with comparison to serum LDH and protein. Transudate has low LDH (<200) and low protein. Pleural to serum LDH < 60% and pleural to serum protein < 50%. * Transudate typically caused by systemic diseases. Exudates typically caused by lung diseases. * Exudate: pleura has some process that causes it to exude fluid. The larger the effusion, the safer the thoracentesis. * Say we do the tap and the LDH is 300 and protein is 3grams (high). This is an exudate. * Exudate causes include cancer, tuberculosis, pulmonary embolus with infarction, pneumonia. If infected material exudes out (parapneumonic), we have a complicated effusion and need a chest tube to drain else it scars and the patient loses lung volume. This scaring can happen quickly. * Complicated exudative effusion (requiring chest tube) includes infection with pH < 7, pus on tap, polys on gram stain, and low glucose in fluid. Next step is chest tube, not antibiotics, not intubation, not further diagnostic studies. * Parapneumonic effusion leaks fluid but no low pH, no pus, no polys on gram stain, not low glucose. So this is an uncomplicated parapneumonic effusion. This patient does not need a chest tube. So patient has fever, pneumonia, and effusion. Next step is put a needle into the space to determine if it is complicated. If not, just treat pneumonia. * Empyema is an effusion with pus in the space, requires a chest tube. -------------------------------------------------------------------------------------------------------------------------------------------Atelectasis * A 62yo man is dyspneic 24hours after cholecystectomy. His respiratory rate is 22, and pulse is 112, has a mild fever, and decreased breath sounds are noted in the left lower lobe. CBC shows leukocytosis of 27,000. * Patient is post-op with anesthesia medication causing decreased lung expansion, is on narcotic meds and likely not taking in deep breaths because of pain. Most likely diagnosis is atelectasis. * Atelectasis is collapsed alveolar airways, lung itself is not condensed on itself. * Massive ascites pressing up on lungs and impairing ability to take deep breath can cause atelectasis. * Broken ribs causing pain on inspiration can cause atelectasis. * This can give rhonci or crackling at the bases, perhaps a little wheezing. * You can get mild fever with atelectasis. Post-op surgical “W”s of fever: Wind (atelectasis), Water (UTI), Walking (DVT), Wound (incision infection), Wonder drugs (drug causes) for days 1, 3, 5, 7, and 9. * Next step in diagnosis is chest x-ray. * Treatment is inspired spirometry breathing device, also known as incentive spirometry.


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Study Notes – Internal Medicine

James Lamberg


-------------------------------------------------------------------------------------------------------------------------------------------Chronic Obstructive Pulmonary Disease (COPD) * Patient has COPD, is a non-smoker, liver problems, and has relatives that died of lung or liver problems. Think alpha-1 antitrypsin deficiency. Patient can have either liver or lung involved, not necessarily both. * Treatment is symptomatically, recurrent antibiotics, hoping they do not need a lung or liver transplant. * COPD patients can develop pulmonary hypertension, giving a loud second sound on heart exam (P2). During inspiration, right-sided heart pressures increase. So here the second heart sound will get louder on inspiration. Patient may have a right-ventricular heave, and ECG may show right-ventricular hypertrophy. * Worry that this patient will develop cor pulmonale. This is similar to CHF in a patient developing left ventricular failure due to hypertension. * Patient with COPD has obstruction so you hear increased wheezing, large AP diameter (barrel chest), and history including smoking, past episodes of bronchitis. * Patient with chronic bronchitis will have increased markings on chest x-ray. Patient with emphysema will have blebs that can become bullae, flattening of the diaphragm, widened silhouette so heart looks smaller, breath and heart sounds may sound very distant. * Pulmonary function tests will be diminished FEV1 and FEV1/FVC ratio. * DLCO test can help differentiate between bronchitic patient and emphysematous patient. There is destruction of the alveolar-capillary membrane in emphysema (low DLCO) but not bronchitis. * In an asthmatic, we give them beta2 agonists acutely and try to keep them well between attacks with steroids. * Ipratropium tends to work better in COPD than asthma for bronchodilitation. * Beta2 agonists help in COPD. Antibiotics for frequent bronchitic infections; They get pneumococcus, h. influenza, moraxella catarrhalis. We use sulfa antibiotics, penicillin antibiotics, cephalosporins, sometimes tetracycline. We try to rotate these antibiotics. So say patient had a good response to TMP-SMX; next choice when they get an infection should be something new else they will develop resistance, so ampicillin or erythromycin. Macrolides (azithromycin) and fluoroquinolones (levofloxacin) also good choices. * Aminophylline is a phosphodiesterase inhibitor with minor bronchodilation effect that has some use in COPD. Toxicities of aminophylline include tachycardia, tachyarrhythmias, tremors, and seizures. We have much better and safer bronchodilators in asthma, namely the beta2 agonists like albuterol. * Aminophylline used in COPD to increase central respiratory drive, improves diaphragmatic contractility, it makes the work of breathing smoother. * Say patient is long-time smoker and getting tachyarrhythmia. Next step is stop theophylline or aminophylline and get an aminophylline level. * Aminophylline is not cleared well in patients on erythromycin, ciprofloxacin, and cimetidine. Drugs that decrease aminophylline levels include warfarin and phenytoin. * Steroids should be monitors. Even with inhaled steroids patient can get cataracts, osteopenia, osteoporosis, hypertension, fluid overload, diabetes, and so on. Demonstrate benefit (baseline PFTs) pre- and post-steroids. * Most patients do not benefit from steroids if you do the measurements before and after a couple of weeks. * Most important treatment for COPD is stopping smoking. Even stopping smoking after decades of damage has benefit. Smoking cessation improves symptoms and mortality. Combine pharmacologic and counseling. * When is the patient hypoxic enough to get chronic home O2? Criteria is PO2 < 55mmHg at rest. If PO2 between 55 and 60mmHg, likely you will be less than 90% oxygen sats. So in this group, look for end organ damage, so erythrocytosis (Hct increased) as a compensatory mechanism or signs of cor pulmonale. * So how much oxygen? It’s cheap, why not just give 100%? These patients have respiratory acidosis, 7.30/50/50, so they have high PCO2, low PO2, “50/50 club.” Home O2 not only makes this patient feel better, it makes them liver longer. We want this patient into the low 90% oxygen sat range. We don’t want to knock out their hypoxemic drive to breath, else we’re in big trouble. This patient is already acidemic, so they need some hypoxia as a central CNS respiratory drive. Otherwise they hypoventilate more, PCO2 goes up, pH goes down. * Typical dose is home O2 1-2L via nasal cannula. * COPD patients should get pneumococcal vaccine every 5 years. They should get influenza virus vaccine annually. They can also get the hemophilus influenza (faintly staining gram negative rod) vaccine once in a lifetime. * What is the most important test for COPD? Answer is FEV1 as a measure of lung disease. -------------------------------------------------------------------------------------------------------------------------------------------Bronchiectasis * Destruction of the elasticity of the bronchial walls, leading to recurrent infections. * Bronchiectasis seen in chronic bronchitis patients and in kids with recurrent infections (tram track sign on chest xray), think about cystic fibrosis.


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

* A Doppler is a valid initial approach in a pregnant patient. * A thrombus is a clot at its point of origin. * Mesothelioma is a specific and rare cancer seen with asbestosis. * In a PE. * Patients develop interstitial lung disease. DO NOT DISTRIBUTE .g. * Treatment is to get patient to stop smoking. since the presence of DVT warrants anticoagulation. diagnosis found via occupational history. An embolus is a broken off clot that traveled. rest of exam is normal. cancer. such as symmetric swollen joints possibly with hand involvement. ABG 7. * Silicosis is seen with rock mining. * 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. Patient breathes in nuclear-labeled air and an image is taken to determine ventilation. * If you see oral contraceptives (hypercoagulability due to estrogen) and sudden chest pain. Normally there is a superimposed pattern of ventilation and perfusion. * Coal miner’s lung associated with mining coal. nearly always fatal. digging quarries. Then IV nuclear material is labeled to RBCs and another image is taken to determine perfusion. * By the time you think to biopsy a cancer. * Encourage patient to quit smoking.08.75 = 45 (normal < 15). * The DVT risk for hip surgery is so high that standard of care includes pre-op prophylactic anticoagulation (subcutaneous heparin. This is rarely necessary. you order a V/Q scan. or high probability of PE.2*25 = 120. waste of ventilation. -------------------------------------------------------------------------------------------------------------------------------------------Pulmonary Embolism (PE) * A 32yo woman is brought to the ED with acute onset shortness of breath and pleuritic chest pain (sharp pain. If you look down and see answer choices like venous Doppler. you should think about rheumatoid arthritis (Kaplan syndrome) and check rheumatoid factor. that is enough to start with anticoagulation. HR > 100. ventilation/perfusion (V/Q) mismatch. then you do the pulmonary angiogram. you will see ventilation but no perfusion in a particular area. * CXR shows calcification of the pleura (white areas). Results come as low. coughing. thing PE. * To detect a V/Q mismatch. Answer is not mesothelioma. A PE usually originates from the deep veins of the legs or pelvis. the airway is just fine. But there is a clot blocking blood in the pulmonary artery. So the problem is with gas exchange. no rhonchi. * Gold standard to detect a PE is a pulmonary angiogram. injection of dye into small vein of the foot with imaging to see the dye. The test is painful. thighs > calves. * Patients at risk for DVT get anticoagulated (subcutaneous heparin) or get sequential compression devices (SCDs). digging tunnels. She has never been sick before. * Another non-invasive test is a Doppler sonogram of the lower extremities. only done if you have no choice. eggshell white.Study Notes – Internal Medicine James Lamberg 28Jul2010 * No specific signs or symptoms. If there is a blood clot. no wheezing. * What is the quickest test to determine if a patient needs treatment for a PE? Answer is Doppler. The radiologist has a large list of criteria to determine probabilities. intermediate. you know it is likely a question about pulmonary embolus. * Patient may be ambulatory but have dementia so they don’t leave bed. * V/Q scan is not gold standard. clinical signs/symptoms of DVT.52/25/75. * Restrictive disease. you may be forced to do more tests. lungs are clear. * What is the first step in detecting a pulmonary embolus? Answer is V/Q scan (non invasive study). Silica fibers are released from rock blasting. Say the Doppler is equivocal and the V/Q scan is equivocal. PE is likely #1 diagnosis. * A-a gradient: 150 1. there will be barbell shaped ferruginous body (asbestos fiber coated with iron-rich material). the alveolus is just fine. ABG shows mild evidence hypoxemia. especially hip replacement). * Pulmonary angiograms are used less widely now due to more acceptance of the spiral CT scan with contrast.19 - . This patient is not taking any medications except oral contraceptives. So there is an area that is ventilated but not perfused. use subcutaneous heparin. * 70-fold increase in primary lung cancer in asbestos exposure with concurrent tobacco smoking. * Gold standard to determine if a patient has a DVT is a venogram. especially if a smoker. Primarily you see thick pleural bases. such as use of oral contraceptives. it is likely too late. So you need to do testing. * Patients with silicosis should get annual PPD testing. If there is a PE. spiral CT scan. is tachycardic. Restrictive disease. Drop PCO2 by 10. and hemoptysis. * Risk factors for pulmonary embolus (Wells criteria): immobilization (e. post-op. previous PE/DVT. worse with deep breath. or moving) that occurred while she was shopping. Her respiratory rate is 26. If you happen to get a biopsy. Detected by biopsy only. pH goes up by 0. CXR nodules favor the upper lobes (similar to TB). * Physical exam will reveal an absence of problems. ventilation perfusion scan. 5000U subq q12h) as well as post-op anticoagulation. small round densities typically mid to lower lobes. * Patients with coal miner’s lung who have joint complaints. With intermediate. These patients are at increased risk for TB. So 120 . Other hypercoagulable criteria are not included in Wells.

* If the patient has a high INR without bleeding. a qualitative problem. or ECG S1 Q3 T3 pattern (abnormal S wave in I. * If a large pulmonary vessel is clotted.7.20 - . If you’re at a PTT of 100. * If the pulmonary embolism makes it peripheral to the pleura. You could see this on CXR possibly. The fastest acting anticoagulation agent is IV heparin. could be a few hundred dollars a day. which will work within the hour. * A patient has a positive V/Q scan with symptoms. Examples are recent major surgery. * Factor V Leiden is the most common cause of thrombophilia. So. right axis deviation on ECG. has a baby pressing on her pelvic veins. * Measure warfarin via PT (prothrombin time. So you want to prevent the clot from getting bigger. so quantitative levels of protein C are normal. so it will not break the clot. IX. VII. still in the presence of a clear lung exam. and is not moving around much. think hypercoagulable state.5 to 2. * FFP comes from other human beings thus it can come with infections and transfusion reactions. more specifically fresh frozen plasma (FFP).Study Notes – Internal Medicine James Lamberg 28Jul2010 * Patient is normally ambulatory busy businessman. * When do you need to know for sure that this is a pulmonary embolus. Q wave in III. So if INR is 1. * We do not start warfarin at the same time as we start the heparin.5 times the control. * Treat patient with IV heparin for about 5 days. IV vitamin K will lower INR in 6-8 hours. * Patients with CHF are at increased risk for DVT/PE due to poor cardiac output and blood stasis. this patient got pregnant and now is hypercoagulable due to estrogen. * Check heparin level with PTT (partial thromboplastin time) test. International normalized ratio (INR) range for a DVT is between 2 and 3. we just follow the dose. So we treat the patient with IV heparin for 5 days then send them home on subcutaneous heparin (10. Heparin is not thrombolytic therapy.5-2. stop heparin for a few hours to let the level come down as patient is at high risk of bleeding. increase heparin infusion rate. you can get signs of right ventricular strain. * Clots in strange places. * Warfarin has a sizeable morbidity and mortality associated with it because there is variation in week-to-week or even day-to-day dosing. Keep patient on continuous heparin infusion.5 times control. Factor V Leiden causes activated protein C resistance. Start patient on oral anticoagulant (warfarin/coumadin) that they will stay on for the next 3-6 months. acute right ventricular heave. * 25yo woman stopped taking her birth control pills because she is scared of clots after reading about them on the Internet. takes long flight across seas and is suddenly short of breath. If INR is 5. protein S. this is most likely a PE case. 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. X. * Heparin works by potentiating antithrombin III effect. recent duodenal bleeding ulcer. give vitamin K. Protein C has the shortest half-life. Once the patient has a stable PTT. loud S2. * So once PTT is 1. we give factors II. it is teratogenic. P2 louder with inspiration. shorter than factor VII. LMWH is a once a day dose. So the first effect warfarin has is to make the patient protein C deficient. and flipped T wave in III. She has been gaining weight and stays at home most days. If control in assay is 30 seconds. we need to reverse the effect of warfarin. IX. so much so that we do not need to follow repeated PTT levels. * Warfarin works by inhibiting vitamin K dependent coagulation factors (II. Subcutaneous vitamin K not recommended. Warfarin inhibits protein C. Warfarin is contraindicated in pregnancy. Aiming for time of 1. Heparin is safe during pregnancy. * The problem with LMWH is that they are very expensive. increase oral warfarin dose to get them above 2 for the DVT. If this patient does get a DVT. the pleura can infarct and cause a pleural rub. Oral vitamin K will lower INR in 24-48 hours. Prothrombin no longer measured directly. recent CVA. May see signs of cor pulmonale acutely. like upper extremities (axillary vein) or in any artery. plus protein C). distended neck veins. Even sitting in a car for a long trip. Heparin is given in bolus (say 5000U) then infusion (say 10 or 15U/kg) at say 1000U/hour. X. Treatment is anticoagulation. “pro time”).000U subq TID as we need 20k to 30k units daily). Protein C and S as well as antithrombin III (AT III) are necessary to prevent constant coagulation. then we can start the warfarin. not specific or sensitive). DO NOT DISTRIBUTE . Pregnancy increases risk for DVT. VII. we have to regularly check INRs. Problem with PT test is control time varies too much. recent major trauma. so they have more tendency toward hypercoagulability. even with a massive PE the CXR will be normal. as many drugs affect the same P450. * Low molecular weight heparin (LMWH) has more consistent effect on PTT. it is done by INR. antithrombin III) to break up the clot and after time the vessel will recanalize. You do not think the patient is going to die from this clot. then we can give heparin. So. INR between 3-4. Factor V is necessary for protein C to work. You expect the patient’s own endogenous system (protein C. * If patient bleeding with high INR. If PTT low. * Drug interactions are important with warfarin. you want 45 to 75 seconds. If for stroke or prosthetic valve. This is not the normal case.

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

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

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

Typical drugs are beta-lactams (e. Treatment is stop drug and short-term steroids to cool down reaction. If you see urine eosinophils. nasal. gold. * Teenager presents with intrinsic renal disease. if you don’t see pre-renal or post-renal problems. If you find post-renal. it is most likely intrinsic renal. * Patient has lung lesions and recurrent sinus infections. sinus.24 - . BUN/Cr is high. * Phases of ATN are prodromal. low specific gravity. urine Na > 20. heavy metal poisoning (lead. Once uncer the bed he couldn’t get out. cancer drugs (cisplatin. hypertension. Had a sore throat a week before. * So in pre-renal BUN/Cr is high with low urine sodium. * Drugs and toxin causes include analgesics (NSAIDs). * In summary. * Deposition disease causes include hemoglobin (hemolysis). Also has kidney issues. treat it. lithium). These patients will lose their oncotic pressure and develop edema. then that may cause high urine sodium do don’t assume intra-renal failure. thrombotic thrombocytopenic purpura. Urine sodium >20-40 because kidneys are failing so they lose the ability to protect sodium. rash. in intra-renal BUN/Cr is low with high urine sodium. not done often in clinical practice because of risk. think allergic interstitial nephritis and look for what drug needs to be stopped. * Treatment for pre-renal azotemia is fluids. urine specific gravity 1. Next thing to do is exclude post-renal azotemia by sonogram and/or catheter looking for lack of obstruction. or treat CHF or renal artery stenosis). mitomycin C). most commonly a cephalosporin.028. like furosemide. Berger disease (IgA mesangial deposition after viral illness. antibiotics (aminoglycosides. Presentation is fever. -------------------------------------------------------------------------------------------------------------------------------------------Intra-Renal Disease: Glomerular Disorders * Vasculitis causes include Wegener granulomatosis (lesions in lung. SLE). Renal biopsy is the most definitive test. cyclosporin. previously called “shock kidney”). * Elderly man dropped pen under bed and went to go retrieve it. penicillins). uric acid crystals (chemotherapy. Think Wegner and order ANCA. you’re faced with a high creatinine level that is new (azotemia). -------------------------------------------------------------------------------------------------------------------------------------------Intra-Renal Disease: Tubulo-Interstitial Disorders * Acute tubular necrosis (ATN) occurs in prolonged ischemia (hypotension. and ANCA anti-neutrophil cytoplasmic antibodies). Henoch-Schonlein purpura. methotrexate. amphotericin B. cephalosporins. Can’t concentrate urine. Osm > 500. rifampin. oxalate crystals (ethylene glycol. sulfonamides. expired tetracyclines leading to Fanconi syndrome).6. which goes through the renal tubules and is toxic to the tubules. * If patient on diuretics. abnormal urinary sediments (hematuria. * Allergic interstitial nephritis is an allergy reaction to a drug. Alport syndrome (renal failure and deftness). urine osmolarity < 350. FENa < 1%. BUN 82. so urine specific gravity < 1. allopurinol. urine Na+ 6.015. cryoglobulin disease. this is 4+ dipstick positive with grams on measurement. RBC casts). * Glomerulonephritis causes include post-streptococcal (do ASO titer. -------------------------------------------------------------------------------------------------------------------------------------------Glomerulonephritis * Intra-renal disease has high urine sodium (> 20) and high FENa (> 1%). urine Na < 10. * Intra-renal azotemia: BUN/Cr is < 10-15. * Algorithm: First thing to do is exclude pre-renal azotemia by looking for lack of BUN/Cr > 20. Key findings are urine eosinophils. Casts come from the kidney. Neighbor realizes man hasn’t come out of the house for a few days and finds the man stuck under the bed. mercury. Osm < 200. granular and RBC. FENa > 1%. collagen vascular disease (e. Has orthostatic hypotension. Answer is order ASO titer. If you find pre-renal. * Nephrotic syndrome occurs in vasculitis and glomerulonephritis. * Patients who have diabetes (and are taking metformin) and get contrast dye should have the metformin stopped prior to the procedure. diabetes. high specific gravity. protein (multiple myeloma with Bence Jones protein).g. cephalosporins. follows strep skin or throat infection). young children). Goodpasteur syndrome (anti-GBM antibodies in lung and kidney). drugs like aminoglycosides and amphotericin B. you treat the cause (most causes you give them fluid. oliguric (when kidney starts showing changes). and post-oliguric (diuretic). peripheral eosinophilia. So. creatinine was normal now is 2. hypercalcemia (hyperparathyroidism). it just leaks out.5g/day. gout). The broken down muscle tissue releases myoglobin. pigments like myoglobin). Massive proteinuria > 3. tumor-lysis. Signs of intra-renal disease are BUN/Cr < 10. Follow azotemia algorithm. prolonged pre-renal azotemia. DO NOT DISTRIBUTE . toxins (radiologic contract.g. vitamin C). radiation nephritis. * Infection causes include pyelonephritis with WBC casts and bacteria in urine. polyarteritis nodosa. Answer to why they are failing is pre-renal azotemia.Study Notes – Internal Medicine James Lamberg 28Jul2010 * 62yo man comes to the ED with nausea and vomiting. urine sodium is low so kidneys are retaining it. Patient has been lying on the big muscles of the legs for a long time with no good circulation. myoglobin (rhabdomyolysis). Also look for casts. arterial insufficiency/occlusion.

Pericarditis occurs due to toxins causing inflammation of the pericardium and build-up in the pericardial sac of fluid. Creatinine is 3.25-dihydroxy vitamin D. Hyperlipidemia also seen. so likely dehydrated. * Best initial test to distinguish causes of intrinsic renal disease is a urinalysis. glomerulonephritis (15%). Could have BPH or cancer causing large prostate obstruction. we assume renal disease and follow that. exam confirms edema. * Chronic manifestations of ESRD occur whether or not you are on dialysis. Best test to establish a diagnosis of nephrotic syndrome is 24-hour urine protein. uric acid (gout). * Need for dialysis is not determined by creatinine level. it’s 20 plus concentrated urine. bicarb is 16 (metabolic acidosis). What is the best initial treatment? You may be tempted to pick sonogram due to outlet obstruction. Best initial treatment is fluids. Most common cause of dialysis is diabetic kidney disease. Could have hypoperfusion due to NSAIDs. Metabolic acidosis occurs but kidneys cannot compensate. RBCs. * Urinalysis can show infection (WBC. BP 110/70. This is an indication for dialysis. BP 140/90 (pretty high). creatinine 3. There is a lack of 1. drug hypersensitivity (eosinophils). can’t dilute urine even though he is vomiting/dehydrated. * 62yo man comes to the ED with nausea and vomiting. It is determined by the presence of acute manifestations. All acute manifestations are indications for dialysis. pulse 110. How do you prove it is nephrotic? 24h urine protein. So pre-renal azotemia. * 14yo boy comes to see you with swollen hands and legs. This causes secondary hypoparathyroidism. no RBCs. What is the best treatment for this patient? Answer is dialysis now. not bicarbonate for acidosis. so need dialysis. high creatine kinase CK in blood). Patient has high pulse and nausea with vomiting. RBC casts. Hypocalcemia with osteopenia occurs. bacteria). no casts.023. Fluid overload occurs to the point of pulmonary edema and the kidneys cannot remove the fluid. 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. Once that is out of the picture.Study Notes – Internal Medicine James Lamberg 28Jul2010 They can run their total albumin way down and get anasarca (“marshmallow man” appearance). Could have bladder cancer or kidney stones due to RBCs in urine.2. think glomerulonephritis. you need dialysis or a transplant. think drug reaction like cephalosporins. This is a clue up front because most people on dialysis get it every 2-3 days. Urine shows proteinuria and RBC casts. * Dialysis can be done via blood (hemodialysis via a machine) or peritoneal dialysis (fluid instilled into peritoneum then removed). the combination of accelerated hypertension and hyperlipidemia leads to accelerated atherosclerosis leading to cardiovascular disease. calcium is leached from bone causing osteopenia. Anemia occurs due to lack of erythropoietin production in the kidneys. Heavy proteinuria. High triglycerides think nephrotic DO NOT DISTRIBUTE . but still need to rule out post-renal. BUN 72. needs dialysis. BUN 41. Exam is normal except large prostate. In order to survive. needs dialysis. BP 11/70. no medications. Cardiac exam shows peripheral edema and signs of CHF. afebrile. Urine Na+ 9. urine sg 1. Hypermagnesemia occurs due to failure to excrete magnesium. * 62yo man comes to the ED for nausea and vomiting. vomiting. What blood test would be most helpful for confirming diagnosis? Answer is ASO titer. * Some key words in renal disease to remember. not to mess around with other treatment. myoglobinuria (blood on dipstick due to myoglobin. not kayexalate for potassium. Exam normal except large prostate. pulse 110. Urine Na+ 42. Encephalopathy occurs at to high creatinine levels. and shortness of breath. usually asymptomatic. and unknown (10-15%). * So you have a patient with azotemia. so must get dialysis. This is likely intrinsic kidney (intra-renal) azotemia. Creatinine is 5. hypertension (10-25%). myeloma (Bence Jones). What is the next step though? Answer is sonogram to exclude post-renal azotemia. If you look at the BUN/Cr. You rule-out pre-renal and post-renal. which is involved in calcium reabsorption in the GI tract. This is post-streptococcal glomerulonephritis. He has a recent sore throat. but a 62yo man probably has a large prostate due to BPH. not furosemide for CHF.6 (new) and is on NSAIDs. and can lead to them being obtunded and even comatose. start to occur when the creatinine gets to about 3. * 62yo dialysis patient returns from a 4-day fishing trip and feels poorly. * Acute manifestations of ESRD include hyperkalemia (look for peaked T-waves on ECG). think nephrotic syndrome. * Most common causes are diabetes (30-50%). -------------------------------------------------------------------------------------------------------------------------------------------End Stage Renal Disease (ESRD) * ESRD is renal failure that is incompatible with survival. Pruritus occurs presumably due to toxins circulating in the blood that are normally excreted by the kidney. glomerulonephritis (RBC casts). So we ruled out pre-renal with urine originally. BUN/Cr is close to 10. Dipstick is positive for protein and patient has edema. Urine sg 1. Immunosuppression occurs so increased infections. ECG shows tall peaked T waves. Patient has nausea.004. nephrotic syndrome (lots of protein).6 (new). Accelerated hypertension (renin-angiotensin action) occurs and is a big deal because it may be hard to control blood pressures. * Best test to determine the type of glomerulonephritis causing the nephrotic syndrome is renal biopsy. Eosinophils in urine.25 - . polycystic kidney disease (5-10%). You see blood in the urine and RBC casts.

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

clofibrate. If there is no response to the ADH. cyclophosphamide. High glucose could cause pseudo-hyponatremia. and has pneumonia. tolbutamide. * 73yo man with COPD and CHF has had diarrhea for 3 days. resulting in quadriplegia. * Symptoms of hypokalemia if mild are asymptomatic. fix pneumonia. The more appropriate term now used is osmotic myelinolysis. glucose 342. it can cause seizures due to cerebral edema. narcotics. * Key points about hyponatremia: determine serum osmolality. various renal diseases). * Drugs that mimic ADH function include oxytocin. Sodium is 126. theophylline. and less commonly in diabetes insipidus (DI) where water loss is up to 20L per day. In diabetes insipidus. -------------------------------------------------------------------------------------------------------------------------------------------Electrolyte Disorders: Hypokalemia * Hypokalemia common causes are GI loss from diarrhea. and if severe and can’t find a reversible cause then demeclocycline or lithium. Then. do a water restriction test. Meds include furosemide and albuterol. * Treatment of central diabetes insipidus is to correct the underlying problem if possible (e. * Emergency treatment for serious hyponatremia is hypertonic saline. meaning urine output drops and becomes more concentrated. Other causes include licorice in high quantities due to mineralocorticoid effect of glycyrrhetinic acid. vinblastine. cardiac arrhythmias occur. beta-agonists (e. Hypothyroid can cause ADH syndrome. seizures. -------------------------------------------------------------------------------------------------------------------------------------------Electrolyte Disorders: Hypernatremia * Hypernatremia is likely the least common of the sodium and potassium abnormalities. digitalis/digoxin toxicity is potentiated. or Bartter syndrome from volume depletion secondary to impaired renal resorption of NaCl. What are the possible causes of hyponatremia? Vomiting could cause dehydration.g. NSAIDs. used in labor induction. and non-specific T and U wave changes. * Drugs to pay attention to here include TCAs. carbamazepine. lithium. phenothiazines. albuterol) that increase potassium entry into cells. muscle cramps. Fluoxetine and chlorpropamide can cause SIADH. stop drug). with low osmolality you need to determine ECF. tube drainage. children).g. brain tumor). Received multiple albuterol treatments in the ED (emergency department). the patient is given ADH. the problem is the kidneys (nephrogenic DI). chlorpropamide. cyclophosphamide. like Conn syndrome primary hyperaldosteronism from renal disorder. At any level of hypokalemia. and the albuterol with increased cellular resorption of potassium. the furosemide with loss of potassium in the urine. * 82yo man presents with 1 week of vomiting and 2 days of confusion. Get a urine osmolality if volume status is normal. vincristine. moderate include muscle weakness. With severe hypokalemia. the urine volume will decrease with time and the urine output will be more and more concentrated. DO NOT DISTRIBUTE . which impairs urinary concentration ability. * Correcting hyponatremia too quickly can cause central pontine myelinolysis. vincristine. there is no change in urine volume because there is no ADH to do it. Takes thyroxin. * Diagnosis of SIADH is accomplished by seeing hyponatremia. Identify three possible causes of hypokalemia. and chlorpropamide.g. In a normal person. * Treatment is to reverse the cause if possible (e. NSAIDS increase prostaglandin (PG1). burns. You also need urine sodium if volume status is low. If you correct the sodium too rapidly. think about diabetes insipidus. If there is a response to the ADH. also medication such as diuretics causing renal loss. MAO inhibitors.Study Notes – Internal Medicine James Lamberg 28Jul2010 *Drugs that increase ADH secretion include TCAs. The urine will not change concentration either. Causes include diarrhea with loss of potassium in the stool. Thiazides cause Na+ depletion and water resorption in the kidney. and insulin that increases potassium entry into cells. * Symptoms include lethargy. low serum osm. * Drugs that increase ADH action include chlorpropamide. and coma. tumor) and nephrogenic causes (lithium. * Rare causes of hypokalemia include hyperaldosteronism. phenothiazines. * If you think the patient has DI. and commonly occurs in GI loss from diarrhea (e. fluoxetine. confusion. * Treatment of nephrogenic diabetes insipidus is to give thiazides or NSAIDs. give vasopressin in the form of desmopressin (DDAVP) usually intranasal or sometimes subcutaneous or IV. high urine osm.27 - . high and normal osmolality are artifacts of high glucose/lipids/protein. furosemide with normal saline (to raise blood sodium). * If you cannot correct the sodium. then the problem is in the brain (central DI). fluoxetine. How do you determine the cause? You need osmolality level and volume status.g. carbamazepine. * Causes include fluid loss in excess of Na+ loss commonly occurs in insensible loss from sweat (extreme exercise). restrict fluids. or Cushing syndrome from adrenal excess. Now has increased SOB (shortness of breath). * Treatment for dehydration is isotonic fluids with slow correction of sodium (1mEq/2h). DI can occur due to central causes (idiopathic. * What is the most common cause of hypernatremia? Answer is dehydration.

42/47/PO2/33/97%. complains of fatigue. early aspirin toxicity. * What if the patient above had an O2 sat of 76%? This is not acute anxiety or panic attack. IV replacement maximum is 10mEq/hour via peripheral IV or 20mEq/hour via central line. and rarely familial periodic paralysis. such as an error in the hospital with excessive potassium administration. leading to falsely high potassium levels. Pseudo-hyperkalemia can occur as an artifact from venipuncture or cell lysis from shaking the blood tubes. ACE-inhibitors). ABG is 7. which can vary by the altitude you live at. low sodium. HCO3 unchanged because not enough time. HCO3 unchanged because not enough time. increased HCO3. never overcompensation. K+ out). RR is 36. Hemolysis of cells causes the potassium to be released from the cells. Labs reveal creatinine increased to 4. Could be a patient on birth control pills with acute pulmonary embolism. This is metabolic alkalosis defined by high pH and high HCO3. PCO2 at 25 is low. * Metabolic alkalosis is either a loss of H+ or a gain of HCO3. This is respiratory alkalosis. and HCO3 of 33 is high. Another causes is deceased renal excretion from renal failure or medications like spironolactone and ACE-Is. pain attack). replace orally. Why did her potassium become high? There are a number of reasons include the ACE-I. * Metabolic alkalosis is a chronic process. Next step is to lower the potassium level by driving potassium into the cells. could be renal failure. O2 sat typically in mid-90s. How will you treat this? * Treatment should start with protection of the heart. * Respiratory alkalosis will have increased pH. ABG shows 7. anxiety (acute pain.43 is alkalosis. * 24yo female comes to the ED feeling like she is suffocating. an inability to blow off CO2. likely due to the hyperventilation. ABG also gives O2 and PO2. You get PCO2 (normal 35-45) and should determine respiratory rate/volume. * Respiratory acidosis has decreased pH. low chloride. sudden cardiac conduction defects preceded by classic ECG changes (talk pointed peaked T-waves). Chronic causes include COPD. increased PCO2. and if sustained the kidneys will retain HCO3 in an attempt to lessen the acidosis. DO NOT DISTRIBUTE . Exam shows orthostatic hypotension. with bicarbonate working as a metabolic buffer. * Respiratory acidosis caused by hypoventilation (acute or chronic). also with bicarbonate as the alkalosis drives potassium into cells. * 67yo woman with diabetes and hypertension is on glyburide and ACE inhibitor.interchange). Drives down the PCO2 with no time for metabolic compensation. with compensatory slowing of respiratory rate and increase in PCO2. They still have potassium in their body but it is no longer in the circulation where it would induce cardiac arrhythmia. HCO3 rises with time to compensate almost back to a normal pH. Acute causes include narcotics. * 67yo woman with HTN is on HCTZ.4 +/. Give CaCl or Ca++ gluconate infusion. should be above 90% normally. So PCO2 of 47 is high. This is a lung problem. Last step is to get rid of the potassium from the body. She presents for a routine checkup. or asthma.5 and potassium is 6.37 is acidosis and pH > 7. * Symptoms include weakness that increases with potassium level. and sleep apnea.0. potassium sparing diuretics. -------------------------------------------------------------------------------------------------------------------------------------------Electrolyte Disorders: Hyperkalemia * Causes include increased potassium intake. * Respiratory alkalosis is caused by hyperventilation. Patients needs treatment if ECG changes present. Potassium is one of the chemicals used for lethal injection because it causes heart block and asystole. these changes are slower (2-5 days). Electrolytes show low potassium. respiratory rate slows to raise PCO2 thereby increasing pH almost back to a normal value. Movement of potassium from cells into the blood can cause hyperkalemia. these changes are rapid. Pickwickian (obesity hypoventilation syndrome). Hyperventilation lowers PCO2 and breath holding or shallow respirations will increase PCO2. rhabdomyolysis. Either way it is a lung problem. Whenever possible. Common causes of H+ loss include prolonged vomiting or other GI loss and diuretics (H+ and Cl.g. occurs in acidosis (H+ into cells. Common causes of HCO3 gain include NaBicarb ingestion (multiple antacid pills) and milk-alkali syndrome (CaCO3). A pH < 7.28 - . This is done with cation-exchange resin (kayexalate) or dialysis if renal failure. * Arterial blood gas (ABG) gives you pH. The PCO2 being high is respiratory compensation. -------------------------------------------------------------------------------------------------------------------------------------------Acid-Base Disorders * A normal blood pH is 7. She appears anxious. Hypoaldosteronism and adrenal insufficiency are other cause. This is done with glucose and insulin. * Metabolic alkalosis has increased pH. decreased PCO2.Study Notes – Internal Medicine James Lamberg 28Jul2010 * Treatment of hypokalemia is done by replacing potassium.03. acute COPD. obesity. pneumonia). This can also occur if blood is drawn proximal to a running IV drip that contains potassium. acute pulmonary disorder (pulmonary embolism.6. has tightness in her throat and chest. An excessive rate causes cardiac conduction defects including heart block and/or asystole.52/25/PO2/27/99%. where you can determine if this is acidosis or alkalosis. You get HCO3 (normal 20-28). This is uncommon except in conjunction with certain medications (e.

paraldehyde/phenformin. Cl 113.3. uric acid. Occurs with aldosterone or adrenal insufficiency and diabetes. Nevada). * Metabolic acidosis is a relative increase in the quantity of acid. * Metabolic acidosis is the most complicated of the group. ethylene glycol. are radiolucent and may not be seen by CT or other x-ray. This is a narcotic overdose with respiratory acidosis due to hypoventilation. Common causes are diarrhea and renal tubular acidosis (RTA). body is breathing fast to bring down PCO2. ABG shows 7. Comes to the ED because she is becoming gradually SOB. or intoxication (ethylene glycol. renal failure (uremia). Inability to acidify urine. idiopathic hypercalciuria. has altered mental status. * Oxalate. * Type 2 RTA occurs in the proximal tubules of the kidney. iron/INH. Anion gap is normally 11 +/. fludrocortisone. Presents with hyperkalemia. Arizona. * Renal tubular acidosis key clue is the inability to acidify urine. * Main causes of struvite stones include infection with urea-splitting bacteria (proteus most common. and struvite have calcium and are radio-opaque.29 - . tissue breakdown (e.9. uremia. Lytes are Na 140. Renal failure causes inability to excrete organic (non-HCl) acids. magnesium/ammonium/phosphate (“triple phosphate” or struvite). pseudomonas). What is the anion gap? Gap is 12. hyperoxaluria (fat malabsorption as fat binds to calcium.4) in the presence of blood acidemia. so likely a CO2 retainer with the COPD. starvation). How do we know this is not primary metabolic alkalosis (i. urine would be inappropriately high pH in RTA. * Main causes of calcium oxalate/phosphate stones include increased calcium absorption (sarcoid. -------------------------------------------------------------------------------------------------------------------------------------------Kidney Stones (Nephrolithiasis) * Urolithiasis occurs in 1-5% of the US population.28/56/PO2/28/84%. with causes including addition of acid. Treatment is mineralocorticoid replacement. * Anion gap < 14 (normal) usually caused by HCO3 loss in GI tract or urine or inability to excrete acid in urine. the body does not overcompensate. amphotericin B. and loss of base (HCO3).g. Respiratory rate is 7. leaving oxalate for excessive absorption). * Metabolic acidosis has decreased pH. * 72yo man has 4 days of diarrhea and presents to ED with weakness. * 17yo with diabetes has not been taking his insulin.g. Normal anion gap acidosis is excess HCl or loss of HCO3. destructive bone disease (myeloma. * Five kinds of stones: calcium oxalate (most common). Is this acidosis or alkalosis? Answer is acidosis. more common in desert southwest (e. phosphate about 10%.3). hematologic malignancies).37 is not alkalosis. PCO2 being low is compensatory. salicyclates. ABG shows 7. diabetic. inc HCO3 with inc PCO2 compensating)? We know this because the pH of 7. * Type 4 RTA occurs due to hypoaldosteronism.29/29/PO2/17/97%. Diagnosed by seeing bicarbonate lost in urine in the face of acidic blood. vitamin D deficiency. Intoxication causes addition of non-HCl acids. Is this metabolic or respiratory? Answer is metabolic acidosis. HCO3 18. * Type 1 RTA occurs in distal tubules of the kidney. What would be the best test to distinguish diarrhea from RTA? Answer is urine pH. vitamin C excess. struvite about 5-10%. Seen in kidney stones. * Must determine which type of metabolic acidosis. metastatic cancer). As compensation. Needle tracks on arms. lithium. * MUDPILES: methanol. Diagnosed by high urine sodium with salt restriction (salt restriction test). lactic acidosis. others). * Anion gap > 14 caused by overproduction or under-excretion of an acid other than HCl. * Main causes of uric acid stones include gout. calcium phosphate. cysteine (rare). Inability to absorb bicarbonate until levels very low. Her PCO2 is high.31/30/PO2/17. Fanconi syndrome. methanol wood alcohol.Study Notes – Internal Medicine James Lamberg 28Jul2010 * 27yo man found unconscious on the street.e.37/5/PO2/34/90%. ABG shows 7. Chloride levels are unaffected “normochloremic. * High anion gap acidosis is an excess of non-HCl acid. Anion gap = (Na + K) – (Cl + HCO3). so 8-14. either high-anion gap (anion gap) or normal anion gap (nonanion gap). Lactic acidosis is due to overproduction of lactic acid. occurs rapidly. phosphate. vitamin D intoxication). * 72yo woman has COPD worsening over weeks. * Oxalate stones account for about 70%. urate about 5%. alkaline urine favors crystallization of struvite and can result in large stones (staghorn calculi). ABG shows 7. hyperparathyroidism. diabetic ketoacidosis.” There are four major causes: ketoacidosis (alcoholic. Seen in myeloma. DO NOT DISTRIBUTE . cysteine rare. lactic acidosis. Treatment is oral bicarbonate. inability to excrete acid. Urate may not be seen on plain x-ray. What is the most likely cause of the this patient’s normal anion gap metabolic acidosis? Most likely diarrhea. Wilson disease. klebsiella. sickle cell. and increased respiratory rate as compensation in an effort to blow off PCO2 thereby increased pH almost back to normal. This is metabolic acidosis as bicarb is low. K 2. urinary pH typically > 5. Pupils small. so normal anion gap (11 +/. Could be RTA. decreased HCO3. Treatment is volume restriction. which should be acidic (< 5. salicylate.4 or even overtly alkaline. * Ketoacidosis is due to overproduction of ketone bodies. Diagnosed by giving acid load/challenge test and still can’t acidify urine.

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

* “White-coat” hypertension is thought to occur in about 20% of cases of diagnosed HTN. Cushing disease will have striae. Patient has no symptoms from left kidney. and basic labs.g. If BP systolic 130-139 or diastolic 85-89. * Investigating secondary causes can be done by history. subarachnoid hemorrhage. If BP systolic 140-159 or diastolic 90-99. then 1 month. * Chronic complications include heart disease with >1million MIs per year. What is the next step in the evaluation. severe headache). hyperthyroid is beta-blockers and anti-thyroids. * High risk groups for HTN include African Americans. then 1 week. physical. Renal failure can be discovered by creatinine level elevation. aldosteronism is aldosterone level. Answer is cyst aspiration/puncture. patient may present with heart attack or retinal hemorrhage. eye disease. enalapril. average of 2 readings. coarctation is ultrasound studies. Sonogram to study gallbladder reveals gallstones. Pheochromocytoma presents with sympathetic episodes. * Hypertensive emergencies need immediate treatment: angina or CHF. * Treatment for hypertensive emergency is nitroprusside infusion. -------------------------------------------------------------------------------------------------------------------------------------------Hypertension (HTN) & Hypertensive Emergencies * Optimal is systolic < 120 and diastolic < 80. * 62yo man is being evaluated for RUQ abdominal pain. * Essential hypertension has no clearly identified cause or reversible process. * Again. * Stage 2 hypertension is systolic 160-179 or diastolic 100-109. polycystic kidney is ACE-I (maybe) and renal transplant. that is 1/4 of the adult population. papilledema. Must do a percutaneous aspiration biopsy (CT needle aspiration). * Chronic complications include CVA (400. * Stage 3 hypertension is systolic 180+ or diastolic 110+. seek end-organ damage. when do you have to get the patient back for a confirmation? If BP systolic > 180 or diastolic > 110. * Ambulatory BP monitoring gives data for a 24h period. confirm on 2 subsequent visits. * Complex renal cysts vary in size. BP is 170/99. renal artery stenosis is angioplasty. rounded moon-facies. * Stage 1 hypertension is systolic 140-159 or diastolic 90-99. 60% of persons over age 65 have HTN and 75% are not controlled. * Say the patient comes back and their HTN is confirmed. seasonal rhinitis spray). bladder encircles 80% or more of arm. CT scan confirms findings. Hyperaldosteronism will come with low potassium. blurred vision). acute eye findings (hemorrhages. Coarctation of the aorta can be found by pulse lag. If BP systolic 160-179 or diastolic 100-109. coarctation is surgical. aortic regurgitation is echocardiogram. then 2 months. a complex cyst is cancer until proven otherwise. pulse striking earlier in radial than femoral arteries.Study Notes – Internal Medicine James Lamberg 28Jul2010 * Complex renal cysts are usually incidental findings on sonogram or CT.000 new CHF per year. * Most common presentation is incidental finding in an asymptomatic individual. Cushing is dexamethasone suppression test and/or cortisol. * What is the best test if a secondary cause is suspected? Medication-induced is stop meds and follow BP. polycystic kidney is renal sonogram. buffalo hump. goiter). do history. creatinine. cerebral impairment (ischemia. * What is the initial treatment if a secondary cause is suspected? Medication-induced is stop meds and follow BP. complex renal cysts are cancer until proven otherwise and need CT-guided needle biopsy. then every other year. pheochromocytoma is VMA and metanephrines and catecholamines. useful for suspected “white coat” hypertension. Renal artery stenosis is found by bruit on abdominal exam or sudden abrupt onset of HTN. Cushing is remove pituitary adenoma. Hypertensive emergency is uncommon. * After you get a first blood pressure reading. murmur. * Hi-normal is systolic 130-139 or diastolic 85-89. but also a small (2cm) cyst on left kidney with complex echos. Also nitroglycerine (with MI). multiple (complex) echos/septations seen on CT or ultrasound. due to some other condition that is often reversible. potassium. * 32yo previously normotensive man sees you for a work physical. renal artery stenosis is captopril renogram in young (fibromuscular) and Doppler flow in elderly (atherosclerotic). Chronic complications can develop. regardless of size. and males > females. labetalol. By definition. Aortic regurgitation has high systolic pressure and low diastolic pressure. exam. then yearly. Perform a physical exam and laboratory investigations to seek secondary causes. and no hematuria. renal failure is BUN/Cr. * BP measurement method: patient resting quietly for 5 minutes. * Epidemiology shows 50million Americans with HTN. diabetics. renal failure (5. Medication causes include birth control pills and alpha-agonists (e. or found during workup of hematuria or abdominal pain. What is the next step in evaluating his blood pressure? Answer is return in 1-2 months. and seek/control atherosclerotic (ASHD) risks.31 - . seated with arm at heart level. If BP systolic < 130 or diastolic < 85. His history and exam are otherwise unremarkable. obese. Normal is systolic < 130 and diastolic < 85. Polycystic kidneys can be found by mass or hematuria. 400.000 strokes/year). Hyperthyroidism can cause HTN (tremor. < 5% of HTN is secondary. * So for secondary HTN causes. hyperthyroid is ultra-sensitive TSH. aldosteronism is DO NOT DISTRIBUTE .000 ESRD/year).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

diff can start to flourish. given oral. He is treated for 7 days with IV cefazolin with dramatic improvement in his symptoms. usually non-bloody. difficile causes a secretory diarrhea. difficile patients do not have sky-high white counts. colonic (left sided abdominal tenderness). gut tries to dilute non-absorbable lactose. so look at medication list for antibiotics. * Treatment is metronidazole first-line. Enterocytes have villi and microvilli with lactase enzyme. terrible neuropathy) use vancomycin. which are yellow exudative plaques on the colon. nurse). campylobacter in the hospital. * Patient do not develop shigella. stools bloody DO NOT DISTRIBUTE . To get stool osmolality 2*(Na + K) so 274 here.g. if cytotoxic then we know it is coming from C. do a toxin assay. you can differentiate osmotic from secretory diarrhea from clinical presentation and initial laboratory testing. close to 274. * 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. Next step is vancomycin. C. With lactase deficiency. * Everyone with pseudomembranes on exam has C. paramedic. receiving antibiotics. Normally C. can wait for toxin assay. diff lives in the lumen of the gut so you want to clear it from the lumen of the gut. appendectomy. * If patient cannot tolerate metronidazole (e. quinidine. Patient may have connection to the medical field (works in drug store. There are also strains of VRE (vancomycin-resistant enterococcus) “superbugs” so metronidazole is first-line. In a negative sigmoidoscopy. Pseudomembranous Colitis * 59yo construction worker is admitted to the hospital for treatment of cellulitis that developed after dropping a steel beam on his leg. and even that is not perfect because the spores are so sticky. * Causes of C. Bacteria can ferment the lactose so patient can get a lot of gas and discomfort as well. * Ways to get C.g. so this is an osmotic diarrhea. * Pseudomembranous colitis associated with a very high white count (e. * Stool Osmolar Gap is a calculation you will probably only see on the boards. Say it is 275. Alcohol-based hand sanitizers do not remove C. Patient may have multiple operations that they don’t have good reason for. * Antibiotic-associated colitis (non-pseudomembranous) is diarrhea associated with the change in flora that occurs with antibiotic use.57 - . spectrum from well with mild diarrhea to very toxic-appearing with high fevers. You may get called to the ICU for a very sick patient who has been on many antibiotics. Think factitious diarrhea. milk sugar. Medication causes include magnesiumcontaining drugs. difficile so hand-washing with soap and running water is required. 3 exploratory laparotomy operations. IV metronidazole gets into blood stream but not really to lumen of the gut. Exam shows vague mile left mid-abdominal pain. like cholecystectomy for vague symptoms. * Young female patient has supposed secretory diarrhea. they don’t want to wait for a few days they want to know now so get your sigmoidoscope and get moving. * Most C. difficile. * Osmotic diarrhea means there is an osmolar substance that is not absorbed in the small intestine. difficile make pseudomembranes. Vancomycin is more expensive than metronidazole. WBC of 30-50. Stop antibiotics in these cases. so gap of 76mosm of something that does not belong there. but if it is present it points you to C. 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. go for sigmoidoscopy. If not very sick. patient is taking laxatives. * Now measure osmolality directly for the stool. gold salts for rheumatoid disease. * Say you measure 2*(Na + K) as 274 and osmolarity is 350. * C. PO (oral) is very effective. etc. or being exposed to diarrhea (nosocomial infection). difficile. even if you’re a gastroenterologist. antibiotics as a side-effect. difficile are being in a hospitalized/nursing home setting.Study Notes – Internal Medicine James Lamberg 28Jul2010 calcitonin. but not all patients with C. difficile colitis includes clindamycin (most likely). So besides the Na+ and K+ there is nothing else that has osmolar properties in the stool. * Direct way to make the diagnosis would be to put a sigmoidoscope in the patient and look for pseudomembranes. Patient in the hospital is likely nosocomial or medications. difficile does not grow in the gut but when you wipe out the normal flora with antibiotics the C. difficile colitis). He has had diarrhea for the past 5 days. So not likely osmotic diarrhea. * In clinical practice.000). There are also strains of vancomycin-resistant staphylococcus. Add stool to plate. If very sick patient. so the small intestine tries to dilute it by adding water into the lumen of the small bowel. salmonella. You’ve done all the studies and hormone assays but found nothing. Also cephalosporins or penicillins because we use those medications more than clindamycin. This appearance does not look like anything else so you can tell the patient right there that they have pseudomembranous colitis. difficile. colchicine. Ischemic Colitis * 72yo man complains of LLQ pain for the past few days. probably secretory. What is your next step in the evaluation of this patient? * Top of the differential list should be pseudomembranous colitis (C. * Most common osmotic agent is lactose.

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

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

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

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

Study Notes – Internal Medicine James Lamberg 28Jul2010 bleeding. Blood is not absorbed in the colon so BUN/Cr would not increased with a straight colonic bleed. * 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. Many people have diverticuli that do not bleed. An angiogram requires active bleeding to be positive. 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. no melena. we generally send the patient to surgery. injected back into the patient. in between) is likely colonic bleeding. then the bleeding scan can help localize the problem area. If the patient continues to bleed. * Medical therapy is not as useful for controlling GI bleeding. In elderly. * A clue that rectal blood is from an upper GI bleed is an increased BUN/Cr ratio. You should not see a blush or collection on the right side. * 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). or during the prep the bleeding could have stopped. but might not be diagnostic. You would see gastric cells light-up in the small bowel. * Diagnosis of Meckel diverticulum done with a bleeding scan that labels gastric mucosa. It is done if the nuclear scan cannot be done or the nuclear scan is not diagnostic. just formed brown stool. * Hematochezia or maroon stool (not BRBPR. * Exception is children or young adults with negative colon testing and painless blood emanating through ileocecal valve. so BUN raises out of proportion to creatinine. then looking for the bleeding source. Say the patient his diverticuli along the whole colon and you see lots of blood on colonoscopy. the aorta and internal iliacs. * A red blood cell scan in the abdomen should show you the vasculature normally. Sigmoidoscopy can be done immediately. * Diverticulosis usually found in sigmoid. It requires more active bleeding than a nuclear scan. BUN/Cr around 40:1 because small intestine absorbs some of the blood and breaks it down to urea. which is why the nuclear scan is done first. * Angiography is rarely used. endoscopist can inject a sclerosing agent or place rubber bands over veins (banding). usually epigastric with/without radiation to back. painless bleeding. associated with nausea and vomiting. Also nuclear scan is less invasive and can be repeated over several hours. type and cross blood. AVMs usually found in ascending right side of colon. Next step if the patient is actively bleeding is a bleeding scan where nuclear label is mixed with the patient’s red blood cells. Treatment is resection. given as IV bolus then hourly infusion typically for three days if the patient has esophageal variceal bleeding.62 - . Alcohol is a direct toxin to the pancreas DO NOT DISTRIBUTE . If the patient stops bleeding from diverticular disease and then restarts. * Say you do flexible sigmoidoscopy and it is non-diagnostic. * Lower GI bleeding is defined as distal to the ligament of Treitz. Pancreatitis * Acute pancreatitis presents as abdominal pain. 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. Exception is variceal bleeding. * The colonoscopy can show the location of the bleed. you should suspect Meckel diverticulum. * If esophageal varices. * Nearly all cases of acute pancreatitis are caused by alcohol or gallstones. * Medical management for esophageal varices specifically is octreotide. AVMs more commonly seen in patients with aortic stenosis (controversial idea). * If the bleeding scan is non-diagnostic and the patient continues to bleed from diverticular disease. called Meckel scan. next most common is diverticulosis then arteriovenous malformations (AVMs. A local external exam or short-scope anoscopy can show hemorrhoids or fissures that are bleeding. which would imply right colon. physician can inject the blood vessel locally with the angiogram catheter or maybe put a coil in to stop the bleeding. You can see anorectal bleeding or on occasion see diverticular bleeding. Octreotide is a synthetic analog of somatostatin and reduces portal pressures. * Most common cause of mild (small amount) painless rectal bleeding is hemorrhoids or fissures. sometimes diffuse tenderness. typicaly AVM. Exam shows tenderness in mid-epigastric region. Endoscopy allows you to make the immediate diagnosis and even treat the source. Bleeding events may be episodic. so if you see them do not assume that was the cause. IV PPIs might help. You do colonoscopy and it is non-diagnostic. * If major bleeding. the surgeon is stuck and has to do a sub-total colectomy taking out the whole colon down to the rectum. but very few things bleed in the small intestine. * Management of choice is endoscopic hemostasis. can be done laparoscopically. Start large bore IV(s). Octreotide is 8 peptides. angiodysplasia was previous name). they require a resection. Gastric mucosa arrives in the diverticulum and acid production can cause ulceration of the diverticulum causing bleeding. * Most diverticular bleeds stop spontaneously and do not require surgery. * During angiography. Hopefully the bleeding scan pinpoints the area for localized resection. so you see the bleeding diverticuli then go higher and see no blood. give fluid. if the cells are leaking out somewhere they will accumulate in that area. next step is stabilization.

That bilirubin is the one that ends up in your bloodstream making you yellow or into kidneys making urine tea or cola colored. pain. * Blood test abnormalities are described in Ranson prognostic criteria. Albumin bound bilirubin coming out of spleen is not water soluble and is not urinated. * Treatment of gallstone pancreatitis that does not resolve on its own is endoscopic retrograde cholangiopancreatography (ERCP) with stone removal. * Mnemonic (48 hours): C HOBBS. Severe pancreatitis is likely if score 3+.63 - . bilirubin producing a yellow color. Indirect is unconjugated bilirubin. Mortality 100% if score 7 or 8. Cholangitis is classically with Charcot triad of RUQ pain. O2. AST. they need surgical debridement of the abscess or even radiology-guided needle aspiration. and jaundice. and hemosiderin producing a golden-brown color. LDH. A stone would need to block either the common bile duct and/or the pancreatic duct (choledocholithiasis). BUN. thus high unconjugated bilirubin will not darken the urine. * Initial labs should include amylase and lipase. which is problematic because in general they are alcohol addicts and you run the risk of making them narcotic addicts from iatrogenic prescribing. * The colors of a bruise are caused by the phagocytosis and sequential degradation of hemoglobin to biliverdin to bilirubin to hemosiderin. after taking in intestinal nutrients. 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. Bilirubin is also metabolized here. now pancreatic enzymes drain right into the jejunum preventing irritation of the pancreas from trapped enzymes. Liver Disease * Liver is an important synthetic site for many compounds such as albumin and coagulation factors. * If patient is not getting better after a few days of NPO and IV fluids for pancreatitis. They can present with endocrine insufficiency as diabetes with insulin dependence from beta cell destruction. NG tube if need to decompress the stomach (if vomiting). * Gallstone pancreatitis never leads to chronic pancreatitis because patient either gets better or goes for stone extraction with ERCP. lipase is more specific. For ICU patients. * RBCs last about 120 days and get trapped in spleen in the reticuloendothelial system as they break down. hematocrit. glucose. * Say total bilirubin is 5. hemolysis). calcium. Procedure filets open the pancreas then sew a loop of jejunum into the bottom of the pancreas. meets with splenic vein into the portal vein and through liver. which was originally developed just for alcoholic pancreatitis.8. Crigler-Najjar. you may need to do follow-up CT scans and drain any new cysts/abscesses. fever. biliverdin producing a green color. IV hydration. Bile and even pus may pour out and patient gets better. and localized pancreatic abscess occurring in a few days. If pancreatic abscess. Pseudocyst can cause obstruction. Bilirubin bound to albumin travels via portal system to liver hepatocytes where it is conjugated to glucuronic acid giving bilirubin glucuronide. sequestration of fluid > 6L. * Inflamed swollen boggy pancreas is called a phlegmon (spreading diffuse inflammatory process with formation of suppurative/purulent exudate or pus). * Total bilirubin is direct + indirect bilirubin. Bilirubin may climb to 5 or 6 here. patient can get an operation called a Puestow procedure. * Gilbert (pronounced jheel-BAYR). * Mnemonic (admission): GA LAW. Then you know most of the bilirubin is unconjugated. WBC count. Chronic pancreatitis is usually associated with alcohol use. * Chronic pancreatitis can present with exocrine insufficiency as maldigestion and we treat them with pancreatic enzyme replacement. exocrine pancreatic insufficiency. All the proteolytic enzymes cannot leave the pancreas so you get autodigestion of the pancreas by the enzymes. do a CT scan to rule out pancreatic abscess.Study Notes – Internal Medicine James Lamberg 28Jul2010 causing inflammation. 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). Calcium becomes deposited through duct system of the pancreas and can be seen on plain film indicating chronic calcifying pancreatitis. with hemoglobin itself producing a red-blue color. and Dubin-Johnson syndrome are problems with indirect DO NOT DISTRIBUTE . It is also an important detoxification organ and nutrition absorption organ. then you know this is not a liver problem (spleen problem. Say total bilirubin is 10 and indirect is 9.0 and indirect is 3. * Treatment is to put the pancreas at rest. * Common bile duct obstruction with cholangitis should be treated via ERCP stone extraction. NPO because food stimulates the pancreas. fistulization into the lung causing pleural effusion (send fluid for amylase). age. * Gallstone pancreatitis is usually associated with a history of biliary colic (crampy RUQ pain after meals). so insulin dependent diabetes but not Type I. * Puestow procedure (longitudinal pancreaticojejunostomy) can be useful to prevent narcotic addition or to help a patient who is already addicted to prescription narcotics. Initial testing can include CT scan. Heme part of RBCs is broken down to biliverdin then to bilirubin. base deficit. Direct is conjugated bilirubin. it is due to chronic pancreatitis. If the pain is very severe. * Treatment for cholangitis should also include antibiotics.

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

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

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

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

Tell them to stop the medication and have their white cells checked. this test is not done anymore so look for a free T4 test. Symptomatic relief includes beta-blocker therapy (propranolol. so you have to follow this patient every six months to check thyroid hormones. We can also use propranolol. Ophthalmopathy is treated separately as patient may not be able to close their eyes and may get eye ulcers. toxic nodular goiter. weight loss. Someone thought this patient might have a thyroid problem. Thyroid hormone is being spilled into the periphery due to destroyed thyroid cells but uptake is low because thyroid is injured. * If agranulocytosis occurs with PTU then you cannot give the patient methimazole. free T4 low. * Management after acute phase is definitive treatment with radioactive iodine to kill the thyroid. and FSH because usually not just one pituitary hormone missing. any changes in albumin and protein levels in the body will fluctuate the total T3 and total T4 levels. weight loss attempt): TSH low. antibodies that affect the TSH thyroid receptors. Example patient with nephrotic syndrome or cirrhosis. So we can only use these at low doses.Study Notes – Internal Medicine James Lamberg 28Jul2010 measure free T4 index. increased FT4. Again. Since this is an ICU patient. menstrual irregularities. Radioactive iodine has not been shown to cause cancer. Within months or years the patient will become hypothyroid. This patient has sick euthyroid syndrome. free T4 normal. intolerance to heat. * With fluctuations in protein the body will keep the free T3 and free T4 stable. Free T4 and TSH would be normal in this patient. or orbit radiation. So be careful when you see a total T4 or total T3 instead of free T4 or free T3. total protein level is down. Resin T3 uptake does not measure T3. * Secondary hypothyroidism: TSH low. they have increased proteins so total T4 will increase. then give thyroid medication (synthroid or any other T4 form). * Complication of PTU and methimazole is agranulocytosis. free T3 elevated. * In pregnant patient with Graves disease the only anti-thyroid medication we can use is PTU. There is no need for endocrine management here. but you definitely DO NOT DISTRIBUTE . The thyroid enlargement is diffuse and is the only time in thyroid disease where you get proptosis and exophthalmos. anything over this is hyperthyroidism. free T4 elevated. It is reversible agranulocytosis as long as you catch it. Normal is 1040% uptake just as a note. * Graves laboratory findings would be low TSH. they will get agranulocytosis with that as well. * A patient is intubated in the ICU and the patient’s FT4 was high or low. then scan the thyroid. free T3 elevated. If patient is on this medication and calls you saying they feel horrible and are running a high fever. free T4 elevated. wait 24h. * Thyroiditis: TSH low. When they become hypothyroid. Example is Graves disease. RAI-uptake scan is low. RAI-uptake scan is low. atenolol) until patient is out of acute phase meaning they feel better and become euthyroid. * Exogenous thyroid medication use (e. antibodies act like TSH to rev-up the thyroid. RAI-uptake scan high. then take the patient to surgery in the second trimester. Example would be pregnant patient or patient taking estrogen. Both of these cross the placenta and have side effects. * Radioactive iodine uptake scan (RAI-uptake) is a way to directly measure function o the thyroid. Is this patient hyperthyroid? No. it is an indirect measure of T4. free T4 elevated. and elevated RAI-uptake if you felt you needed it. Free T4 in this patient would be normal and TSH would be normal.g. bruit over thyroid. Anything under this would be hypothyroidism. but TSH came back normal. The cause is an immune process. RAIuptake scan low or normal. Likely to have abnormal growth hormone. RAI-uptake scan normal. free T4 low. * Proptosis and exophthalmos commonly gets worse when you treat Graves disease. * Anti-microsomal antibodies sometimes associated with Hashimoto disease. Total T3/T4 would be down in this patient but it is not hypothyroid. palpitations. treatment is to wait.9% of thyroid hormones are bound to albumin. Give them a little bit of PTU and propranolol to cool down the thyroid. Example is hypopituitarism. free T3 elevated. * Other Graves signs include dermopathy. diarrhea. or steroids. So they may need surgery. * Since 99.68 - . LH. * Thyroid globulin immunoglobulin sometimes associated with Graves disease. * Primary hyperthyroidism: TSH low. * Pregnancy or protein-increasing medication: TSH normal. Hyperthyroidism * Graves disease is the most common cause of hyperthyroidism. sometimes swelling of the feet (pretibial myxedema). tremor. Radioactive iodine is given to the patient. elevated total T4. Anti-thyroid medications are propylthiouracil (PTU) and methimazole to decrease thyroid hormone level. Example is subacute thyroiditis. tachycardia. Propranolol can cause small for dates. This patient should not be treated with antithyroid medication. free T3 normal. * Management in the acute phase is to relieve symptoms and reduce peripheral thyroid hormone. they likely have a lot of other comorbid conditions. repeat in 48h to see what the uptake is. Thyroid hormones use to be in weight reduction medication a few decades ago even in this country.

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

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

6. Treatment is usually not necessary. With vitamin D deficiency and in some stages of chronic renal failure the parathyroid hormone becomes ineffective. This would be a nursing home patient who is in bed most of the time. so that is a case when you could give calcitonin at the same time as a bisphosphonate. wears off after 48hrs) or bisphosphonates (long acting) like pamidronate. the other three glands shrink due to negative feedback with calcium. * Most of vitamin D is absorbed in the summertime due to sunlight activation. think about hypoparathyroidism. * Older individual with mild asymptomatic hyperparathyroidism may be watched. so majority is protein bound. Example is squamous cell lung cancer or esophageal cancer. What is this patient’s real total calcium? Answer is (4mg/dL . PTH level would be elevated only in primary hyperparathyroidism. * To distinguish in a hypercalcemia patients between primary hyperparathyroidism and hypercalcemia of malignancy. only give furosemide if evidence of overload. Furosemide does not do much to the calcium level. * Fibrosa cystica (brown tumors) develops in the bone due to the constant osteoclast activation resulting in cyst formation. Fluids is the cornerstone of treatment for hypercalcemia. On the other hand. Hypocalcemia * Whenever you see hypocalcemia. Severe hypercalcemia occurs with > 15mg/dL and is a medical emergency. Patient has hypercalcemia with severe peptic ulcer disease and diarrhea. This is the cause of the hypercalcemia (and more phosphorus too). Treat hypercalcemia with fluids (normal saline) primarily. and parathyroid tumors. After surgery. It is a chronic granulomatous disease. but their ionized calcium would remain the same. They will have an elevated calcium level and it is not likely cancer or hyperparathyroidism. Squamous cell cancer does not metastasize much.5 + 1. * Familial hypocalciuric hypercalcemia is a benign disorder. you order PTH level. polydipsia.2mg/dL) = 2 * 0.8 factor = +1. where granulomas occur mainly in the lung but can occur anywhere. no need for medications or further testing. * Furosemide and diuretics can be seen in hypercalcemia protocols because furosemide gets rid of calcium. In 15-20% of cases there is four gland hyperplasia or parathyroid cancer.8. Treatment here is IV calcium with ECG monitoring for QT abnormalities. giving diuretics if calcium is high or if kidney stones occur uncommon. Do not write for IVF and furosemide at the same time here. so hypervitaminosis D. * Hypercalcemia of immobilization is also benign. * Hypocalcemia prolongs the QT interval. this may be due to a gastrin producing pancreatic tumor (Zollinger-Ellison) with parathyroid tumor. So sarcoid patients develop hypervitaminosis D in the summertime or when they go to sunny areas. abdominal pain. it is given because the mainstay of treatment is fluids and we do not want to cause fluid overload in an elderly patient. * Mild hypercalcemia would be bone pain.Study Notes – Internal Medicine James Lamberg 28Jul2010 there is a single adenoma. Watch these patients closely in a telemetry unit and monitor calcium levels for a couple of days. osteitis fibrosa cystica. it grows focally. * With one gland hyperplasia. * Treatment is surgery for definitive treatment. * A patient with nephrotic syndrome would have a lower total calcium.71 - . When we measure calcium in serum we get total calcium and 40% of this is ionized.5. * With hypocalcemia. For every drop in albumin by a single point there is a drop in calcium of 0. So 6.6 = 8. These are breakdown of bone. then calcitonin (immediate action. DO NOT DISTRIBUTE . then watching the serum calcium go up and down. hydrochlorothiazide retains calcium. putting one in the arm.1 total calcium. Lab would be low phosphate. The other mechanism is through production of PTH-like molecule. such as multiple myeloma. make sure to account for low albumin states. * Normal albumin is 4mg/dL. So patient goes from hypercalcemia to hypocalcemia. A patient who got exploratory surgery around the neck area could have had damage to parathyroid gland circulation. pituitary tumors. this is called hungry bone syndrome. Diffuse granulomas seem to activate vitamin D. * Sarcoidosis can cause hypercalcemia. * Primary hyperparathyroidism associated with MEN-I (the 3 Ps): pancreatic tumors. polyuria. * Most blood assays only check for parathyroid hormone that is intrinsic. Treatment is just to monitor the patient. So PTH-like substance may not be picked up by parathyroid hormone levels. These patients hardly ever have symptoms. * Four gland hyperplasia requires removing all four glands. it should be done in all patients with symptomatic hyperparathyroidism such as kidney stones. Ionized calcium is the part that affects neuromuscular irritability. Hypocalcemia after surgery for primary hyperparathyroidism is due to calcium going to bone and nothing left to stabilize the calcium. * Hypercalcemia associated with cancer is usually severe. you have three glands that are not working well. Say nephrotic patient is 2mg/dL albumin and total calcium level is 6. If calcium is still high. Hypercalcemia of Malignancy * Hypercalcemia of malignancy can occur through multiple metastases to bones. Hypercalcemia causes shortened QT. which activates the osteoclast.

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

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

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

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

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

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

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

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

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

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

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

fever. Vincristine and vinblastine causes peripheral neuropathy. This is the ristocetin test (artificial endothelial surface). Adriamycin gives cardiac toxicity. Why don’t we just chemo everyone? Side effects. Hepatitis B vaccine is made this way too. What would you do next in the management of this patient? Stage is IIIb so do chemotherapy with ABVD/MOPP. * TTP is associated with renal failure and hemolysis. vagina)? * Hemophilia: normal PT. so it is not unusual to see prolonged PTT in von Willebrand disease. Factor VIII and vWF sit in the endothelial lining. so increased in ITP. so in the 26yo patient so most likely von Willebrand since it is the most common hereditary coagulopathy. factor-type bleeding. but you need a bone marrow biopsy to see these. So do bleeding time when you see platelet type bleeding with a normal platelet count. where it is made and stored. If you have platelets and ristocetin with vWF present they will stick. This rapidly brings up the vWF level. * How do you do bleeding time? You put on a BP cuff to occlude the veins of the arm. PT is normal. It is not hemophilia because she is a woman. Fibrin is broken to D-dimers (fibrin parts) by plasmin. Factor XIII helps preserve the clot. Cryoprecipitate is pooled blood products and can transmit disease. normal platelets. * Radiation of local disease results in a cure 90% of the time. Tissue plasminogen activating factor (tPA) so that the plasminogen turns into plasmin and then the plasmin chops up the fibrin linked clot. * If you wanted to know how many beers someone drank. 1% will develop aplastic anemia. coli and recombinant technology. Cisplatin causes nephrotoxicity and ototoxicity. platelet count of 217. but enough so the artery is open. * 32yo woman with a neck mass. Fibrin split products gets split off from fibrinogen to activate it to fibrin. * Desmopressin releases sub-endothelial stores of vWF. PTT is prolonged at 52s. * Vitamin K deficiency: prolonged PT. von Willebrand disease. with factor-type and platelet-type bleeding. normal platelets. skin. They are made with E.000.83 - . The spleen is not enlarged on exam. * Say you have platelet-type bleeding with normal platelet count. weight loss. * Factor VIII antigen (vWF) travels bound to the factor VIII coagulant portion (hemophilia). hematoma in muscle) or platelet bleeding (superficial like epistaxis. * Busulfan and bleomycin cause pulmonary fibrosis. * They tell you the spleen is normal to rule-out splenic sequestration. Her prothrombin time is normal at 11s. normal platelets. leading to good clotting. give factor VIII replacements because it comes with some von Willebrand factor (vWF). prolonged/normla PTT. Then you take a razor blade and cut the patient. What is the treatment? Steroids. * After the initial clot is formed via vWF with platelets and endothelium. normal PTT. If DDAVP does not work. * Von Willebrand disease: normal PT. you could look at the empty beer bottles (D-dimer) or the bottle caps that were split off (fibrin split products). * Glanzmann thrombasthenia and Bernard-Soulier syndrome are rare. MOPP. * Treatment of von Willebrand disease is desmopressin (DDAVP). * Factor replacements (VIII. What is the next test for diagnosis? Answer is antiplatelet antibody test. * Treatment of Hodgkin lymphoma is ABVD/MOPP. mucosa. * Megakaryocytes are precursors to platelets. then you might give cryoprecipitate. gums. If that doesn’t work. increased PT. * First thing to do with a bleeding question is determine the nature of the bleeding before you look at the labs. To see if there is functional vWF.000) because bleeding time will always be abnormal. * DIC has low platelets. you need an artificial endothelial surface. Bleeding Disorders * 26yo woman presents with epistaxis and petechiae. Then you time the bleeding.Study Notes – Internal Medicine James Lamberg 28Jul2010 * Treatment of non-Hodgkin lymphoma is CHOP. ABCD) is sterility in 95% of patients. DO NOT DISTRIBUTE . prolonged PTT. Cyclophosphamide causes hemorrhagic cystitis. so do not do a bleeding time if the platelet count is low (< 50. * In order for platelet and endothelium to stick to each other they need vWF. increased PTT. If vWF is not there. * 26yo with platelet-type bleeding. PTT normal. Pelvic CT scan is positive for lymph nodes consistent with lymphoma. What is the next step in management with the assumption of von Willebrand? Answer is bleeding time (prolonged). platelet-type bleeding. * Most common side effect of chemotherapy (CHOP. the platelets do not stick to ristocetin. factor-type bleeding. * It is not vitamin K deficiency because PT is normal. Then get a von Willebrand factor level. 1% a year develop AML. This is idiopathic thrombocytopenic purpura (ITP). Excision biopsy shows Reed-Sternberg cells. What is the most likely diagnosis? This is platelet-type bleeding with a normal platelet count. Bleeding time is a test of platelet function. Testicles are more vulnerable to this effect. night sweats. IX) are clean because they are no longer pooled blood products. fibrin come in and cross-links the clot. Is this factor related bleeding (deep like hemarthrosis in joint. platelet count low. thus it is not used much.

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

Study Notes – Internal Medicine

James Lamberg


* Arthrocentesis: non-inflammatory (osteoarthritis/DJD) has WBC < 2,000/mL, inflammatory (RA) has WBC from 5,000 to 50,000/mL, septic joint has WBC > 75,000/mL. * Say patient has RA with symmetry except for a knee that is 3x larger than the other knee. Arthrocentesis shows WBC 100,000/mL, so that joint is also infected. * Treatment for mild RA is aspirin or NSAIDs, both shown to be as effective. * Major complication of aspirin (ASA) and NSAIDs is upper GI ulcer and bleed. This is still a cause of death in the elderly. Aspirin toxicity at high dose can cause tinnitus and high anion-gap metabolic acidosis that is also associated with a respiratory alkalosis (increased respiratory drive). Interstitial nephritis is an uncommon complication of aspirin. NSAID complications also include renal insufficiency, especially in the elderly who can be dry. NSAIDs can affect CNS, confusion and delirium in high doses. * Acetaminophen is not an anti-inflammatory, thus it is not used in inflammatory disease like RA. Side-effects of acetaminophen (APAP, paracetamol) include liver toxicity and does not cause upper GI ulcers. * Arachidonic acid is metabolized to phospholipase into 2 pathways, cyclooxygenase (COX) and lipoxygenase. Products of COX are prostaglandins and prostacyclin. Products of lipoxygenase are leukotrienes, which are proinflammatory. Prostaglandins mediate inflammation and pain. Prostaglandins are also cytoprotection mediators in the stomach and are helpful for renal blood flow. * COX comes in COX-1 and COX-2. Cytoprotection in stomach is part of COX-1. Renal vasoconstriction is part of COX-1 blocking. Inflammation and pain are part of COX-2. Thus blocking only COX-2 would relieve the pain and inflammation while preventing COX-1 renal vasodilation and maintaining COX-1 cytoprotection. * Celecoxib is a COX-2 selective inhibitor. Rofecoxib was pulled from the U.S. market in 2004. * Treatment for RA should not include long-term steroids because of complications. Steroids are used in the shortterm for a patient that is not relieved with aspirin or NSAIDs. * Disease modifying anti-rheumatic drugs (DMARDs) include gold, penicillamine, azathioprine, and methotrexate. The most useful drug is methotrexate for long-term maintenance of RA. * Methotrexate (MTX) side-effects include liver fibrosis, cirrhosis particularly with cumulative high doses, pulmonary hypersensitivity reaction, bone marrow suppression. * RA patient presents with fever, pleuritic chest pain, infiltrate, and is on DMARD therapy. Answer is stop the methotrexate and give steroids for pulmonary hypersensitivity reaction. * What lab test should you following in a RA patient on long-term MTX? Answer is LFTs and CBC. * Any patient on MTX should also be on folate to help reduce the risk of bone marrow suppression. * Steroid toxicity is common so might as well put steroids on the problem list if a patient is taking them long term. * Steroid toxicity includes cataracts, glaucoma, psychosis, personality disturbances (anxiety, depression, moodlability), uncommon CNS infections like Listeria monocytogenes meningitis (not seen in immunocompetent), candidal thrush, moon facies (big, round), osteopenia and osteoporosis even at a young age, aseptic necrosis (avascular necrosis, osteonecrosis), increased risk of GI bleed. * Osteoporosis with steroids is dependent on dose and duration of steroid use. * Lab test abnormalities with steroids include metabolic alkalosis and hyperglycemia. * Rheumatoid arthritis patient presents with a swollen painful calf. There is no palpable cord and the patient has no risk factors for DVT. This is ruptured Baker cyst in the popliteal space. No need to do diagnostic tests here. * Patient presents after a motor vehicle accident. They have a history of rheumatoid arthritis. What should you be careful of during intubation? Do not hyperextend the neck due to chance of atlantoaxial joint (C1-C2) subluxation. Systemic Lupus Erythematosus (SLE) * 35yo woman is brought for the evaluation of confusion for a day. Her friends and family inform you that she did not know how to get home from work and lately she has not been herself. You find that the patient has elevated blood pressure, decreased air entry at the right lung base with dullness to percussion (pleural effusion), and symmetrical joint swelling of the wrists and MCPs. Chemistry profile shows an elevated creatinine to 2.4 and there is protein in the urine on urinalysis. What blood test might you use to confirm your suspicion? * Anti-mitochondrial antibodies seen in primary biliary cirrhosis (PBC). * Anti-histone antibodies seen in drug-induced lupus. * Anti-double stranded DNA antibodies seen in lupus, particularly specific in active lupus with renal involvement. * Anti-centromere antibodies seen in scleroderma (CREST). * Anti-smooth muscle antibodies seen in autoimmune hepatitis. * Anti-nuclear antibodies (ANA) is very sensitive in lupus, so it will be positive in most cases of SLE but there are many false-positives. If ANA is negative though, it helps rule out lupus. * You rarely see a patient with lupus that has joint involvement as their chief complaint. * Ratio is about 10:1 women to men for lupus.


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Study Notes – Internal Medicine

James Lamberg


* Symptoms of lupus include CNS (lupus cerebritis causing change in mental status, change in personality, depression, psychosis, seizures), alopecia, malar “butterfly” purple rash, discoid lupus (purplish disc-shaped discoloration usually after sun exposure), aphthous ulcers, pleural effusions (lupus serositis), pericardial effusion, sterile vegetation on heart valves (less common, Libman-Sacks endocarditis), renal disease (glomerulonephritis which is hallmarked by RBC casts in urine and proteinuria in nephrotic range), recurrent second trimester abortions due to hypercoagulability from anti-phospholipid antibody (lupus anticoagulant) causing placental vessel thrombosis, joints typically symmetric with arthralgias more than arthritis. * Labs abnormalities for lupus include mild leukopenia, anemia of chronic disease, autoimmune hemolytic anemia, autoimmune thrombocytopenia (decreased platelets, ITP), renal insufficiency (increased creatinine), RBC casts and protein in urine. * Serology for lupus includes positive ANA (peripheral rim pattern), anti-DS DNA, low complement level (CH50) particularly with active lupus nephritis, less likely is anti-Ro (SSA) and anti-LA (SSB) antibodies. * Anti-Ro antibody is associated with neonatal lupus (mother has anti-Ro), babies get complete heart block. * Drug induced lupus causes include hydralazine, procainamide, isoniazid, alpha methyl-dopa. * These patients have prominent serositis, so pleural effusions and pericardial effusions. * Symptoms include arthralgias, fever, fatigue, no CNS involvement, no kidney involvement. * Patient presents with pleural effusion, fever, joint soreness, malar rash, increased creatinine, personality changes. They are taking hydralazine for hypertension. What antibody should you check? Answer is anti-DS DNA because this is true lupus and not drug-induced. Drug-induced would not have CNS or kidney involvement. * Test for drug-induced lupus is anti-histone antibodies. These patients can get false positive VDRLs, they will not have a positive FTA (fluorescent treponemal antibody). * Treatment of SLE is complicated and usually done by the rheumatologist. Know basic drugs though. * Treatment of SLE is NSAIDs for arthralgias and serositis. Steroids used for CNS involvement, kidney involvement, and autoimmune hematologic problems. With nephritis, if steroids are not enough add cytotoxic drugs like cyclophosphamide or azathioprine. * Treatment for SLE with second trimester abortions includes aspirin or low molecular weight heparin to preserve the pregnancy and prevent a thrombotic event. * Treatment for SLE includes liberal use of sunscreens. Scleroderma * 36yo woman comes to you because of skin tightness and painful fingertips with exposure to cold. These symptoms have occurred for over one year. Exam notes tight skin on the face with a shiny appearance. BP is 165/100. Laboratory tests reveal a macrocytic anemia and elevated creatinine. What is the diagnosis? Scleroderma. * Scleroderma is more common in women. * Painful fingertips with exposure to cold is Raynaud phenomenon, which is not unique to scleroderma. Color changes can occur (white, blue, red). Sensitivity can be so exquisite the patient cannot walk into a room that has air conditioning running without their hands becoming painful. Patients may wear gloves in the summer time or be unable to hold a cold iced drink. * Sclerodactyly is skin tightness of the fingers that is so tight it causes bone resorption. * Progressive systemic sclerosis (PSS) is a term to denote scleroderma patients with the most severe disease. Renal involvement is the organ to worry about here and can lead to death, not seen in CREST syndrome. * CREST syndrome is the milder form of scleroderma. * CREST: calcinosis (calcium deposits), Raynaud phenomenon, esophageal hypomotility (severe reflux), sclerodactyly, telangiectases (usually on face). * Esophageal smooth muscle and LES replaced with collagen, leading to worse GERD you may ever see. * Renal involvement in PSS is exacerbated by elevated blood pressure. This is because the renal arteries are replaced by collagen and cannot dilate appropriately, so low renal blood flow due to sclerosis of the renal vessels. The kidneys behave as if they are pre-renal (vasoconstricted), triggering the RAAS pathway. * Treatment of choice for scleroderma with hypertension is ACE-I (lisinopril, captopril, ramipril) to block RAAS. If the patient cannot tolerate ACE-I (e.g. cough), give angiotensin II receptor blocker (ARB) like losartan. * ACE-I cough is an allergic phenomenon related to bradykinin alterations. * 36yo woman with scleroderma, has painful fingers, horrible GERD, hypertension, calcinosis. What is the most important symptom to treat? Answer is treat hypertension aggressively; this is critical to prevent renal crisis. * Treatment should not involve steroids, they are not beneficial in scleroderma and have major side-effects. * Treatment for scleroderma is ACE-I primarily for hypotension. * Treatment for scleroderma can includes penicillamine (some skin manifestations) and calcium channel blockers like nifedipine or nitrates (Raynaud phenomenon).


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Study Notes – Internal Medicine

James Lamberg


Sjögren Syndrome * 42yo woman presents with some peculiar symptoms that she has had over the past year or so. She informs you that she feels there is constantly something in her eyes like dust or sand. She says dry and solid foods are painful to swallow. You are perplexed by her complaints but decide to examine her and find that she has bilateral parotid enlargement but otherwise an unremarkable examination. An ANA test is positive. What specific ANAs do you expect to be positive in this patient? * Triad of dry eyes, dry mouth, and parotid gland enlargement is Sjögren syndrome, an autoimmune disease. * Sjögren syndrome sometimes found by itself, often found in association with other autoimmune diseases such as lupus, rheumatoid arthritis, and scleroderma. A combination of diseases is considered a mixed connective tissue disease (MCTD). These patients tend to have an antibody known as anti-RNP (ribonucleoprotein). * Diagnosis is suspected based on clinical presentation, reinforced with anti-RNP if associated with MCTD. * Schirmer test measures moisture in the eyes (decreased tears). Biopsy of salivary glands shows lymphocytic infiltration. ANA can be positive, also anti-Ro, and anti-LA antibodies. * Treatment is symptomatic with artificial tears and sucking candies, not usually a majorly disabling disease. Ankylosing Spondylitis * 27yo man presents with complaints of severe lower back pain and stiffness that have been bothering him for the past five years. He informs you that the stiffness is more apparent in the morning when he awakes, lasting sometimes for more than two hours. The only thing improving these problems is exercise. On exam he has a 2/4 diastolic murmur over the second right intercostal space and decreased range of motion of the lumbar spine. What is the most likely diagnosis? Ankylosis spondylitis. * Ankylosis spondylitis also associated with sacroiliitis, fusion of the SI joint. The first x-ray finding may be this fusion, suspected when there is this presentation and pain in the pelvic girdle area. This is associated with IBD; the two conditions (IBD and ankylosing spondylitis) can follow independent courses. * Not many pains improve with exercise, this is one of them. RA spares the back, so even though there is morning stiffness you can basically rule out RA. * Seronegative arthropathies (spondyloarthropathies) are more common in men than women. These often have prominent extra-articular manifestations. Genetic marker HLA-B27 positive in most of these. * Aortic insufficiency often seen in ankylosing spondylitis, unknown cause. * There is typically a lumbar lordosis and thoracic kyphosis in normal patients. Ankylosing spondylitis patients lose this curvature giving a straight spine. Lumbar lordosis is lost first, then thoracic kyphosis. Typically the neck is spared or involved only later in the disease progression. These patients walk hunched over with a straight back, associated with a lot of discomfort. * Over time, AP x-ray of spine shows squared-off vertebral bodies and loss of intervertebral spaces. This is referred to as bamboo spine or bamboo shoot spine. * We do not know what causes ankylosing spondylitis and we do not have medications to reverse it. * Treatment is NSAIDs (not steroids), physical therapy, IBD treatment if needed, supportive therapy. Reactive Arthritis (Reiter Syndrome) * Patients get an arthritis as a reaction to an infection elsewhere in the body. Infections usually non-gonococcal urethritis (NGU) like chlamydia and infectious diarrheas (campylobacter most common, yersinia, shigella). * Reactive arthritis usually small joints like hand, usually symmetric. * Symptoms include conjunctivitis, oral ulcers, genital ulcers, urethritis. * Mnemonic: “can’t see, can’t pee, can’t climb a tree” for conjunctivitis, urethritis, arthritis. * Blood test to look for in this clinical situation is HLA-B27. * Treatment for NGU reactive arthritis is treat underlying infection and treat arthritis with NSAIDs. * Treatment for diarrheal reactive arthritis is to treat invasive diarrhea cause (prior to getting arthritis). * Do not make the diagnosis of reactive arthritis unless you know what the arthritis is reacting too. Psoriatic Arthritis * Severe destructive erosive changes in the MCP, PIP, and DIP joints. * HLA-B27 positive, more prevalent in men than women. * Symptoms include prominent pitting of the nails, psoriatic skin changes, psoriatic patches on the scalp. Swelling of the fingers can lead to a condition referred to as sausage fingers. * Treatment with some success is methotrexate. Enteropathic Arthritis * Enteropathic arthritis seen with inflammatory bowel disease. * This does follow a similar clinical course to the underlying IBD (ankylosing does not). * Arthritis is typically symmetric, small joints, hands.


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

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

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

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

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

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

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

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

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

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

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

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

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

if your highest point to attain is the exam it will feel painful. What could it be? Hyperkalemia. The pointier the worse. * The most important ECG to know is regular sinus rhythm. * When talking about peaked T-waves. The peaked T-waves are so high that the monitor is reading them as QRS complexes. -------------------------------------------------------------------------------------------------------------------------------------------- DO NOT DISTRIBUTE . then the exam will feel smaller and your process will be filled with more joy.Study Notes – Internal Medicine James Lamberg 28Jul2010 she missed her dialysis treatment this week.101 - . * Keep in mind when you are studying for the exam. 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.

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