Study Notes – Internal Medicine

James Lamberg

28Jul2010

Textbooks: Cecil Essentials of Medicine, Hospital Medicine Secrets, First Aid for Medical Clerkship Introductory Guide: Primer to the Internal Medicine Clerkship 2nd Edition by Picchioni -------------------------------------------------------------------------------------------------------------------------------------------Common Problems in Internal Medicine Cardiovascular: Acute Coronary Syndromes, Congestive Heart Failure, Valvular Heart Disease, Atrial Fibrillation and Anticoagulation, Hypertension Endocrine: Diabetes Mellitus, Hypothyroidism, Hyperthyroidism, Osteoporosis, Disorders of Calcium Metabolism Hematology: Anemia, Coagulopathies Gastro: Hepatitis, Peptic Ulcer Disease, Gastroesophageal Reflux Disease, Diarrhea and Constipation Oncology: Hematological Malignancy, General Care of the Cancer Patient, Management of Pain Nephrology: Electrolyte Disturbances, Acid-Base Disorders, Acute and Chronic Renal Failure Rheumatology: Rheumatoid Arthritis, Osteoarthritis, Monoarthritides, Polyarthritides Pulmonary: DVT and Pulmonary Embolism, Chronic Bronchitis and Asthma, Emphysema Infectious: Fever of Unknown Origin, Acquired Immune Deficiency Syndrome, Pneumonia, Urinary Tract Infection, Cellulitis, Subacute Bacterial Endocarditis Allergy: Urticaria Neurology: Cerebrovascular Disease, Headache, Dementia and Coma Dermatology: Dermatological Manifestations of Chronic Medical Disease -------------------------------------------------------------------------------------------------------------------------------------------Procedures: NEJM Videos In Clinical Medicine: http://www.nejm.org/multimedia/videosinclinicalmedicine -------------------------------------------------------------------------------------------------------------------------------------------Kaplan Videos (2001) – Board Studying Thoughts from Dr. Conrad Fischer, MD * For USMLE Step 2 (and any exam for that matter), think from the point of view of the question writer. Questions you can expect include “Which of the following is the most likely diagnosis?” seem commonly in Internal Medicine sections, where physicians ponder over the diagnosis for hours. Diagnosis questions account for about 20-30%, more in Internal Medicine, less on Surgery. “Which of the following is the best initial diagnostic test?” or “What would you do first to confirm your diagnosis?” Also, “What is the best diagnostic test” or “What is the most accurate diagnostic test?” Treatment questions follow “Which of the following is the best initial therapy?” Always ask “What is the next best step in the management of this patient?” * What is the problem? Pay attention to the question. If the question asks what is the best initial diagnostic test and you pick the best test (most accurate), you missed the question. If the question asks what is the best initial therapy and you choose the best therapy (most effective), you missed the question. * But you think to yourself, no no no I don’t do this. I won’t make this mistake. But, you do make this mistake because everybody makes this mistake. Examination results show this time and time again. * Answer questions based on what the question-writer is saying, now what you think they mean. * You’re sitting there looking up at that board exam and all you see is a huge exam. You feel scared and all you can think about is how big that exam is. But, if you could find a way to look past the exam and see good and beauty. You could connect with the goodness and beauty that is beyond the exam, which you can’t do right now because all you see is a giant exam. But, if you can connect with the knowledge, the data that you need for the exam and connect it with the beauty and good, great things will happen. * First, the exam will seem much smaller and lighter in the palm of your hands (from William Blake). Second, you will be able to remember the knowledge longer and help someone later on with it, and that is a great good. Third, you will get a better grade anyway and get what you want. If doing well on the exam is your highest aspiration, it will become so painful. Fourth, your trip/voyage/journey will be filled with much more joy. This idea is the analgesic for your studying. -------------------------------------------------------------------------------------------------------------------------------------------How To Succeed In Clerkship – First Aid For The Medicine Clerkship (Stead, Stead, & Kaufman) Be On Time: Team rounds usually begin between 7am and 8am. Give yourself at least 10 minutes per patient for pre-rounding to learn about events that occurred overnight or lab/imaging results. Dress In A Professional Manner: Regardless of what the attending wears. A short white coat should be worn over your professional dress clothes unless it is discouraged (e.g. pediatrics). Act In A Pleasant Manner: The medical rotation is often difficult, stressful, and tiring. Smooth out your experience by being nice to be around. Smile a lot and learn everyone’s name. Don’t be afraid to ask how your resident’s weekend was. If you do not under- stand or disagree with a treatment plan or diagnosis, do not “challenge.” Instead, say “I’m sorry, I don’t quite understand, could you please explain…” Show kindness and compassion toward your patients. Never participate in callous talk about patients.

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Study Notes – Internal Medicine

James Lamberg

28Jul2010

Take Responsibility: Know everything there is to know about your patients: their history, test results, details about their medical problem, and prognosis. Keep your intern or resident informed of new developments that they might not be aware of, and ask them for any updates you might not be aware of. Assist the team in developing a plan; speak to radiology, consultants, and family. Never give bad news to patients or family members without the assistance of your supervising resident or attending. Respect Patient’s Rights: 1) All patients have the right to have their personal medical information kept private. This means do not discuss the patient’s information with family members without that patient’s consent, and do not discuss any patient in hallways, elevators, or cafeterias. 2) All patients have the right to refuse treatment. This means they can refuse treatment by a specific individual (you, the medical student) or of a specific type (no nasogastric tube). Patients can even refuse life- saving treatment. The only exceptions to this rule are if the patient is deemed to not have the capacity to make decisions or understand situations, in which case a health care proxy should be sought, or if the patient is suicidal or homicidal. 3) All patients should be informed of the right to seek advanced directives on admission. Often, this is done by the admissions staff, in a booklet. If your patient is chronically ill or has a life-threatening illness, address the subject of advanced directives with the assistance of your attending. More Tips: Volunteer, be a team player, be honest, and keep patient information handy. Present In An Organized Manner: “This is a [age]-year-old [gender] with a history of [major history such as HTN, DM, coronary artery disease, CA, etc.] who presented on [date] with [major symptoms, such as cough, fever, and chills] and was found to have [working diagnosis]. [Tests done] showed [results]. Yesterday, the patient [state important changes, new plan, new tests, new medications]. This morning the patient feels [state the patient’s words], and the physical exam is significant for [state major findings]. Plan is [state plan].” -------------------------------------------------------------------------------------------------------------------------------------------Presenting A Chest Radiograph (CXR): 1) Technique: Rotation, anteroposterior (AP) or posteroanterior (PA), penetration, inspiratory effort. 2) Bony structures: Look for rib, clavicle, scapula, and sternum fractures. 3) Airway: Look for tracheal deviation, pneumothorax, and pneumomediastinum. 4) Pleural space: Look for fluid collections, which can represent hemothorax, chylothorax, and pleural effusion. 5) Lung parenchyma: Look for infiltrates and consolidations: These can represent pneumonia, pulmonary contusions, hematoma, or aspiration. The location of an infiltrate can provide a clue to the location of pneumonia: * Obscured right (R) costophrenic angle = Right lower lobe * Obscured left (L) costophrenic angle = Left lower lobe * Obscured R heart border = Right middle lobe * Obscured L heart border = Left upper lobe 6) Mediastinum: Look at size of mediastinum—a widened one (> 8 cm) goes with aortic dissection. Look for enlarged cardiac silhouette (> 1⁄2 thoracic width at base of heart), which may represent congestive heart failure (CHF), cardiomyopathy, or pericardial effusion. 7) Diaphragm: Look for free air under the right hemidiaphragm (suggests perforation). Look for stomach, bowel, or nasogastric tube (NGT) above diaphragm (suggests diaphragmatic rupture). 8) Tubes and lines: * Identify all tubes and lines. * An endotracheal tube should be 2cm above the carina. Common mistake is right bronchus intubation. * A chest tube (and proximal hole) should be in the pleural space (not in the lung parenchyma). * An NGT should be in the stomach and uncoiled. * The tip of a central venous catheter should be in the superior vena cava (not in the right atrium). * The tip of a Swan–Ganz catheter should be in the pulmonary artery. * The tip of a transvenous pacemaker should be in the right atrium. -------------------------------------------------------------------------------------------------------------------------------------------Presenting A Chest Radiograph (Mnemonic Method): Mnemonic: RRR, RIP, ABCDEFGH * Right: patient, procedure, date * Rotation: spinous processes are to line up vertically, equal space between clavicles * Inspiration: should show 8 ribs * Penetration: spinous processes should just be visible through the vertebrae * Airway: carina and tracheal deviation * Bones: look at clavicles, vertebrae, scapula, and ribs for fractures

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Study Notes – Internal Medicine

James Lamberg

28Jul2010

* Cardiac silhouette: > 1/2 total chest width could be CHF, determine if edges are clear * Diaphragm: elevated or depressed, right should be higher, no air under diaphragm * Effusions: check borders and edges for fluid levels, hemothorax, atelectasis, pneumothorax * Fields: infiltrates, masses, objects, size (large in emphysema, small in chronic bronchitis) * Gadgets: ET tubes, central lines, chest tubes, pacemakers, ECG monitors, mention this after RRR RIP in ICU * Hilum: any masses or disturbances -------------------------------------------------------------------------------------------------------------------------------------------Presenting An Electrocardiogram (ECG): 1) Rate: The rate is [number of] beats per minute (bpm): * The ECG paper is scored so that one big box is 0.20 seconds. These big boxes consist of five little boxes, each of which is 0.04 seconds. * A quick way to calculate rate when the rhythm is regular is the mantra: 300, 150, 100, 75, 60, 50 (= 300 / # large boxes), which is measured as the number of large boxes between two QRS complexes. Therefore, a distance of one large box between two adjacent QRS complexes would be a rate of 300, while a distance of five large boxes between two adjacent QRS complexes would be a rate of 60. * For irregular rhythms, count the number of complexes that occur in a 6-second interval (30 large boxes) and multiply by 10 to get a rate in bpm. 2) Rhythm: The rhythm is [sinus]/[atrial fibrillation]/[atrial flutter] or other: * If p waves are present in all leads and upright in leads I and aVF, then the rhythm is sinus. Lack of p waves suggests a disorganized atrial rhythm, a junctional rhythm, or a ventricular rhythm. A ventricular rhythm (V Fib or V Tach) is an unstable one (could spell imminent death), and you should be getting ready for advanced cardiac life support (ACLS). * Normal sinus rhythm is usually a regular narrow-complex rhythm with each QRS complex preceded by a p wave. 3) Axis: The axis is [normal]/[deviated to the right]/[deviated to the left]: * If I and aVF are both upright or positive, then the axis is normal. * If I is upright and aVF is upside down, then there is left axis deviation (LAD). * If I is upside down and aVF is upright, then there is right axis deviation (RAD). * If I and aVF are both upside down or negative, then there is extreme RAD. 4) Intervals: The [PR]/[QRS] intervals are [normal]/[shortened]/[widened]: * Normal PR interval = 0.12 to 0.20 seconds: * Short PR is associated with Wolff–Parkinson–White syndrome (WPW). * WPW syndrome is characterized by a “delta” wave, or slurred up-stroke of QRS complex. * Long PR interval is associated with heart block of which there are three types: * First-degree block: PR interval > 0.20 seconds (one big box) * Second-degree (Mobitz type I or Wenckebach) block: PR interval lengthens progressively until a QRS is dropped. * Second-degree (Mobitz type II) block: PR interval is constant, but one QRS is dropped at a fixed interval. * Third-degree heart block: Complete AV dissociation Normal QRS interval ≤ 0.12 seconds: * Prolonged QRS is seen when the beat is initiated in the ventricle rather than the sinoatrial node, when there is a bundle branch block, and when the heart is artificially paced with longer QRS intervals. Prolonged QRS is also noted in tricyclic overdose and Wolfe–Parkinson–White syndrome. 5) Wave morphology: A. Ventricular hypertrophy: There [is/is no] [left/right] [ventricular/atrial] hypertrophy: * There are multiple criteria for determining right (RVH) and left ventricular hypertrophy (LVH). Clues for LVH: * RI>15mm, RI,II or aVF >20mm, RaVL>11mm, RV5 or RV6 >26mm, RI +SIII >25mm, R+S in Vlead>45mm, SV1 +RV5 or RV6 >35mm Clues for RVH: * RV1>7mm, SV1<2mm, R/S ratio inV1 >1, RAD of 110deg or more B. Atrial hypertrophy: * Right atrial hypertrophy: tall or peaked p waves in limb or precordial leads * Left atrial hypertrophy: broad or notched p waves in limb leads C. Ischemic changes: There [are/are no] S-T wave [depressions/elevations] or [flattened/inverted] T waves. Presence of Q wave indicates an old infarct. D. Bundle branch block: There [is/is no] [left/right] bundle branch block. Clues: * Presence of RSR’ wave in leads V1-V3 with ST depression and T wave inversion goes with RBBB. * Presence of notched R wave in leads I, aVL, and V4-V6 goes with LBBB.

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effective antimicrobial therapy.S. 7) Pituitary tumors cause problems for patients by two main mechanisms: mass effect. 22) Transmission of Borrelia burgdorferi (the causative agent of Lyme disease) from an infected Ixodes tick to a susceptible human requires the tick to have fed on the human for at least 40 hours. elimination of secondary infections.Study Notes – Internal Medicine James Lamberg 28Jul2010 -------------------------------------------------------------------------------------------------------------------------------------------Top 100 Secrets – Medical Secrets (4th. regardless of the blood low-density lipoprotein (LDL) cholesterol level. 8) A key concept in evaluating patients with hyperfunctioning endocrine tumors is that biochemical diagnosis should always precede anatomic localization. and both hepatitis A and B are indicated. 2) Acute pulmonary embolism (PE) is a difficult diagnosis to establish despite newer advances in imaging. low HDL cholesterol levels. which applies pressure to surrounding structures. 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. is Streptococcus pneumoniae. CAD-equivalent diseases. 12) Diabetics and patients with vascular disease should be treated with a statin lipid-lowering drug to prevent heart disease and stroke. 10) The most common presentation of hypogonadism is erectile dysfunction and decreased libido in men and amenorrhea and infertility in women. or diabetes should be treated aggressively to reach the LDL-cholesterol target of 100 mg/dL. Zollo) 1) The treatment of severe sepsis syndrome should be based on efficient resuscitation. 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. 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. 17) In patients with Coccidioides immitis infections. influenza. hypertension. in addition to routine adult immunizations. 18) Patients who present with flaccid paralysis during the summer months should be evaluated for West Nile virus infection. The one exception is patients with pituitary/hypothalamic dysfunction. in whom TSH cannot reliably to assess thyroid function. euglycemia. (2) chest CT can help detect most PEs. which results in excessive secretion of a particular anterior pituitary hormone. 5) In the newly diagnosed HIV patient. immunizations against pneumococcal pneumonia. and establishment of therapeutic goals. and (3) a negative Doppler venous ultrasound of the legs does not exclude the diagnosis of PE. early targeted and specific drug therapy. and rising titers suggest worsening disease. higher titers of complement-fixing antibodies suggest more extensive disease. IV catheters should be removed and ophthalmologic examinations performed to evaluate for the presence of retinal disease. 13) The goal blood pressure is < 130/80 mmHg in hypertensive subjects with diabetes mellitus and/or chronic kidney disease. 6) Metabolic syndrome is diagnosed on the basis of abdominal obesity. 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. since it is the most sensitive measure of thyroid function in the majority of patients. 21) In patients with disseminated candidiasis. keep in mind the prudent use of key diagnostic tests: (1) rapid d-dimer by ELISA is an effective screening test. DO NOT DISTRIBUTE -4- . 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). and endocrine hyperfunction. and fasting hyperglycemia. hypertriglyceridemia. age (from 40 to 79 years). 9) The best initial screening test for evaluation of thyroid status is the TSH. 3) In the approach to suspected PE. or gender. 4) The most common etiologic agent implicated in acute bacterial meningitis in the U. approximately 50% of cases are diagnosed post mortem. 11) All patients with coronary artery disease (CAD).

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

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

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

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

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

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

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

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

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

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

Study Notes – Internal Medicine

James Lamberg

28Jul2010

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

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Study Notes – Internal Medicine

James Lamberg

28Jul2010

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

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Study Notes – Internal Medicine

James Lamberg

28Jul2010

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

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

small round densities typically mid to lower lobes.52/25/75. * If you see oral contraceptives (hypercoagulability due to estrogen) and sudden chest pain.g. * What is the quickest test to determine if a patient needs treatment for a PE? Answer is Doppler. Silica fibers are released from rock blasting. * Patients at risk for DVT get anticoagulated (subcutaneous heparin) or get sequential compression devices (SCDs).2*25 = 120. you know it is likely a question about pulmonary embolus. Patient breathes in nuclear-labeled air and an image is taken to determine ventilation. you will see ventilation but no perfusion in a particular area. pH goes up by 0. rest of exam is normal. such as use of oral contraceptives. digging tunnels. * A-a gradient: 150 1. * In a PE. diagnosis found via occupational history. spiral CT scan. lungs are clear. waste of ventilation. * V/Q scan is not gold standard. DO NOT DISTRIBUTE . PE is likely #1 diagnosis. This is rarely necessary. She has never been sick before. -------------------------------------------------------------------------------------------------------------------------------------------Pulmonary Embolism (PE) * A 32yo woman is brought to the ED with acute onset shortness of breath and pleuritic chest pain (sharp pain. worse with deep breath. you should think about rheumatoid arthritis (Kaplan syndrome) and check rheumatoid factor. nearly always fatal.19 - . it is likely too late. So 120 . Say the Doppler is equivocal and the V/Q scan is equivocal. * What is the first step in detecting a pulmonary embolus? Answer is V/Q scan (non invasive study). Drop PCO2 by 10. Results come as low. * To detect a V/Q mismatch. So the problem is with gas exchange. is tachycardic. that is enough to start with anticoagulation. The test is painful. Restrictive disease. the airway is just fine. * Restrictive disease. digging quarries. * Risk factors for pulmonary embolus (Wells criteria): immobilization (e. especially hip replacement). Primarily you see thick pleural bases. no rhonchi. Answer is not mesothelioma. * The DVT risk for hip surgery is so high that standard of care includes pre-op prophylactic anticoagulation (subcutaneous heparin. injection of dye into small vein of the foot with imaging to see the dye. CXR nodules favor the upper lobes (similar to TB). But there is a clot blocking blood in the pulmonary artery. ABG 7.75 = 45 (normal < 15). use subcutaneous heparin. previous PE/DVT. no wheezing. Normally there is a superimposed pattern of ventilation and perfusion. Then IV nuclear material is labeled to RBCs and another image is taken to determine perfusion. With intermediate. the alveolus is just fine. * Pulmonary angiograms are used less widely now due to more acceptance of the spiral CT scan with contrast. * Mesothelioma is a specific and rare cancer seen with asbestosis. This patient is not taking any medications except oral contraceptives. ventilation/perfusion (V/Q) mismatch. HR > 100. * Encourage patient to quit smoking. or high probability of PE. * Patient may be ambulatory but have dementia so they don’t leave bed.08. * Patients with coal miner’s lung who have joint complaints. * By the time you think to biopsy a cancer. you may be forced to do more tests. A PE usually originates from the deep veins of the legs or pelvis. there will be barbell shaped ferruginous body (asbestos fiber coated with iron-rich material).Study Notes – Internal Medicine James Lamberg 28Jul2010 * No specific signs or symptoms. * A Doppler is a valid initial approach in a pregnant patient. * Another non-invasive test is a Doppler sonogram of the lower extremities. or moving) that occurred while she was shopping. ABG shows mild evidence hypoxemia. * Gold standard to determine if a patient has a DVT is a venogram. * Silicosis is seen with rock mining. only done if you have no choice. * Treatment is to get patient to stop smoking. So you need to do testing. * Gold standard to detect a PE is a pulmonary angiogram. * A thrombus is a clot at its point of origin. * CXR shows calcification of the pleura (white areas). such as symmetric swollen joints possibly with hand involvement. Detected by biopsy only. clinical signs/symptoms of DVT. especially if a smoker. and hemoptysis. * 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. These patients are at increased risk for TB. post-op. If there is a PE. If you look down and see answer choices like venous Doppler. thing PE. eggshell white. since the presence of DVT warrants anticoagulation. Her respiratory rate is 26. If you happen to get a biopsy. The radiologist has a large list of criteria to determine probabilities. * 70-fold increase in primary lung cancer in asbestos exposure with concurrent tobacco smoking. then you do the pulmonary angiogram. thighs > calves. ventilation perfusion scan. If there is a blood clot. intermediate. So there is an area that is ventilated but not perfused. cancer. you order a V/Q scan. 5000U subq q12h) as well as post-op anticoagulation. coughing. * Patients develop interstitial lung disease. Other hypercoagulable criteria are not included in Wells. * Physical exam will reveal an absence of problems. An embolus is a broken off clot that traveled. * Patients with silicosis should get annual PPD testing. * Coal miner’s lung associated with mining coal.

* If patient bleeding with high INR. INR between 3-4. then we can give heparin. * A patient has a positive V/Q scan with symptoms. * If the pulmonary embolism makes it peripheral to the pleura. recent major trauma. recent duodenal bleeding ulcer. Examples are recent major surgery. and is not moving around much. * So once PTT is 1. so it will not break the clot. even with a massive PE the CXR will be normal. “pro time”). Prothrombin no longer measured directly. 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. give vitamin K. If this patient does get a DVT. Treatment is anticoagulation. * Warfarin has a sizeable morbidity and mortality associated with it because there is variation in week-to-week or even day-to-day dosing.5 times control. * If a large pulmonary vessel is clotted. it is teratogenic. * FFP comes from other human beings thus it can come with infections and transfusion reactions. * 25yo woman stopped taking her birth control pills because she is scared of clots after reading about them on the Internet. Factor V Leiden causes activated protein C resistance. so quantitative levels of protein C are normal. * Drug interactions are important with warfarin. Start patient on oral anticoagulant (warfarin/coumadin) that they will stay on for the next 3-6 months. Pregnancy increases risk for DVT. increase oral warfarin dose to get them above 2 for the DVT. If you’re at a PTT of 100. LMWH is a once a day dose. this patient got pregnant and now is hypercoagulable due to estrogen. VII. If control in assay is 30 seconds. we need to reverse the effect of warfarin. Once the patient has a stable PTT. which will work within the hour.20 - . Heparin is safe during pregnancy. You do not think the patient is going to die from this clot. Protein C and S as well as antithrombin III (AT III) are necessary to prevent constant coagulation. * We do not start warfarin at the same time as we start the heparin. so they have more tendency toward hypercoagulability. * Heparin works by potentiating antithrombin III effect. So you want to prevent the clot from getting bigger. Heparin is given in bolus (say 5000U) then infusion (say 10 or 15U/kg) at say 1000U/hour. Warfarin is contraindicated in pregnancy. protein S. * The problem with LMWH is that they are very expensive. plus protein C). and flipped T wave in III. right axis deviation on ECG. Q wave in III. Warfarin inhibits protein C. * If the patient has a high INR without bleeding. not specific or sensitive). X. a qualitative problem. If PTT low. Protein C has the shortest half-life. this is most likely a PE case. or ECG S1 Q3 T3 pattern (abnormal S wave in I. think hypercoagulable state. Even sitting in a car for a long trip. you can get signs of right ventricular strain. This is not the normal case. Heparin is not thrombolytic therapy. You could see this on CXR possibly. * Measure warfarin via PT (prothrombin time. we have to regularly check INRs. * Warfarin works by inhibiting vitamin K dependent coagulation factors (II. we just follow the dose. So.5 times the control. So the first effect warfarin has is to make the patient protein C deficient.Study Notes – Internal Medicine James Lamberg 28Jul2010 * Patient is normally ambulatory busy businessman. Subcutaneous vitamin K not recommended. * Low molecular weight heparin (LMWH) has more consistent effect on PTT. distended neck veins. increase heparin infusion rate. Keep patient on continuous heparin infusion. DO NOT DISTRIBUTE . could be a few hundred dollars a day. VII. International normalized ratio (INR) range for a DVT is between 2 and 3. * Patients with CHF are at increased risk for DVT/PE due to poor cardiac output and blood stasis. still in the presence of a clear lung exam. recent CVA. we give factors II. If for stroke or prosthetic valve. * Clots in strange places. * Check heparin level with PTT (partial thromboplastin time) test. loud S2. She has been gaining weight and stays at home most days. then we can start the warfarin. So we treat the patient with IV heparin for 5 days then send them home on subcutaneous heparin (10.5-2. Aiming for time of 1. antithrombin III) to break up the clot and after time the vessel will recanalize. The fastest acting anticoagulation agent is IV heparin.7. * When do you need to know for sure that this is a pulmonary embolus. IX. P2 louder with inspiration. Problem with PT test is control time varies too much. * Treat patient with IV heparin for about 5 days. stop heparin for a few hours to let the level come down as patient is at high risk of bleeding. * Factor V Leiden is the most common cause of thrombophilia. as many drugs affect the same P450. If INR is 5. the pleura can infarct and cause a pleural rub. You expect the patient’s own endogenous system (protein C. Factor V is necessary for protein C to work. acute right ventricular heave. So.5 to 2. Oral vitamin K will lower INR in 24-48 hours. more specifically fresh frozen plasma (FFP).000U subq TID as we need 20k to 30k units daily). X. so much so that we do not need to follow repeated PTT levels. you want 45 to 75 seconds. takes long flight across seas and is suddenly short of breath. it is done by INR. has a baby pressing on her pelvic veins. IX. So if INR is 1. shorter than factor VII. like upper extremities (axillary vein) or in any artery. May see signs of cor pulmonale acutely. IV vitamin K will lower INR in 6-8 hours.

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

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

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

follows strep skin or throat infection). collagen vascular disease (e. Answer to why they are failing is pre-renal azotemia. gout). Berger disease (IgA mesangial deposition after viral illness. Neighbor realizes man hasn’t come out of the house for a few days and finds the man stuck under the bed. and post-oliguric (diuretic). FENa > 1%. If you find post-renal. thrombotic thrombocytopenic purpura. granular and RBC. * Patient has lung lesions and recurrent sinus infections. DO NOT DISTRIBUTE . Signs of intra-renal disease are BUN/Cr < 10. Typical drugs are beta-lactams (e. cyclosporin. expired tetracyclines leading to Fanconi syndrome). it just leaks out. oliguric (when kidney starts showing changes). tumor-lysis. which goes through the renal tubules and is toxic to the tubules. gold. Henoch-Schonlein purpura. If you find pre-renal. mitomycin C). * So in pre-renal BUN/Cr is high with low urine sodium. if you don’t see pre-renal or post-renal problems. * Drugs and toxin causes include analgesics (NSAIDs). myoglobin (rhabdomyolysis). * Nephrotic syndrome occurs in vasculitis and glomerulonephritis. cephalosporins. * Infection causes include pyelonephritis with WBC casts and bacteria in urine. urine specific gravity 1. Can’t concentrate urine. Had a sore throat a week before. peripheral eosinophilia. drugs like aminoglycosides and amphotericin B. sulfonamides. toxins (radiologic contract.g. urine osmolarity < 350.5g/day. Patient has been lying on the big muscles of the legs for a long time with no good circulation. arterial insufficiency/occlusion. radiation nephritis. RBC casts). Alport syndrome (renal failure and deftness). sinus. or treat CHF or renal artery stenosis). * Algorithm: First thing to do is exclude pre-renal azotemia by looking for lack of BUN/Cr > 20. * Deposition disease causes include hemoglobin (hemolysis). * In summary. you’re faced with a high creatinine level that is new (azotemia). diabetes. Next thing to do is exclude post-renal azotemia by sonogram and/or catheter looking for lack of obstruction. BUN 82. These patients will lose their oncotic pressure and develop edema. urine Na > 20.6. Follow azotemia algorithm. penicillins). * Teenager presents with intrinsic renal disease. oxalate crystals (ethylene glycol. most commonly a cephalosporin. -------------------------------------------------------------------------------------------------------------------------------------------Intra-Renal Disease: Glomerular Disorders * Vasculitis causes include Wegener granulomatosis (lesions in lung. heavy metal poisoning (lead. FENa < 1%. If you see urine eosinophils. Think Wegner and order ANCA. Has orthostatic hypotension. high specific gravity. think allergic interstitial nephritis and look for what drug needs to be stopped. * Patients who have diabetes (and are taking metformin) and get contrast dye should have the metformin stopped prior to the procedure. hypertension.24 - . in intra-renal BUN/Cr is low with high urine sodium. abnormal urinary sediments (hematuria. -------------------------------------------------------------------------------------------------------------------------------------------Intra-Renal Disease: Tubulo-Interstitial Disorders * Acute tubular necrosis (ATN) occurs in prolonged ischemia (hypotension.015. Also look for casts. Treatment is stop drug and short-term steroids to cool down reaction. urine Na+ 6. allopurinol. nasal. * Elderly man dropped pen under bed and went to go retrieve it. lithium). rifampin. Presentation is fever. methotrexate. So. previously called “shock kidney”). urine sodium is low so kidneys are retaining it. hypercalcemia (hyperparathyroidism). Answer is order ASO titer. then that may cause high urine sodium do don’t assume intra-renal failure. amphotericin B. * Allergic interstitial nephritis is an allergy reaction to a drug. Key findings are urine eosinophils. not done often in clinical practice because of risk. * Glomerulonephritis causes include post-streptococcal (do ASO titer. rash. SLE). urine Na < 10. cancer drugs (cisplatin. * Intra-renal azotemia: BUN/Cr is < 10-15. Urine sodium >20-40 because kidneys are failing so they lose the ability to protect sodium. antibiotics (aminoglycosides. polyarteritis nodosa.028. Casts come from the kidney. mercury. Osm < 200. * If patient on diuretics. like furosemide. and ANCA anti-neutrophil cytoplasmic antibodies). Once uncer the bed he couldn’t get out. so urine specific gravity < 1. Also has kidney issues. BUN/Cr is high.Study Notes – Internal Medicine James Lamberg 28Jul2010 * 62yo man comes to the ED with nausea and vomiting. cephalosporins. creatinine was normal now is 2. treat it. it is most likely intrinsic renal. pigments like myoglobin).g. -------------------------------------------------------------------------------------------------------------------------------------------Glomerulonephritis * Intra-renal disease has high urine sodium (> 20) and high FENa (> 1%). Massive proteinuria > 3. * Phases of ATN are prodromal. protein (multiple myeloma with Bence Jones protein). prolonged pre-renal azotemia. Renal biopsy is the most definitive test. cryoglobulin disease. you treat the cause (most causes you give them fluid. The broken down muscle tissue releases myoglobin. * Treatment for pre-renal azotemia is fluids. uric acid crystals (chemotherapy. this is 4+ dipstick positive with grams on measurement. vitamin C). Goodpasteur syndrome (anti-GBM antibodies in lung and kidney). Osm > 500. young children). low specific gravity.

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

with a normal amount of sodium. Urine Na+ < 10. BUN/Cr > 20x normal. ADH is secreated causing the patient to retain fluid and excrete concentrated urine. think pre-renal and give fluids. where sodium falls 1. 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. Radiologic contrast. There is a magnitude effect. in the healthy patient there is a small amount of protein/lipid per block of blood. and hypothyroidism. * “Real” hyponatremia is lab hyponatremia (from a basic metabolic panel) with low osmolality. Diagnoses to consider are congestive heart failure. the glucose is about 300mg/dL high. Serum osm is 292 (normal). May be a drug side effect. * Low osmolality with hypervolemia. Thus sodium is normal so the glucose explains this pseudo-hyponatremia. think Goodpasteur. So per unit of blood. there is less sodium even though the concentration has not changed. We have low sodium with normal osmolality. * Low osmolality with euvolemia.26 - . Sodium is gained. also known as psychogenic polydipsia). edematous conditions. such as in high osmolality of hyperglycemia (1. Hemoptysis. the patient is fluid overloaded and the cause is almost always an edematous condition.g. thyroid function. Total protein is 7. nephrotic syndrome. urine osm is high/concentrated. If ECF is low (hypovolemia). there are multiple causes including SIADH. * Patient presents with weakness. where sodium level measures low but artifacts from other substances make it appear low. lab artifact from hyper-trigleridemia or hyperproteinemia (e.6mg% sodium per 100mg% glucose). With moderate change. accompanied and exceeded by secondary water gain. multiple causes).6 per 100mg/dL increase in glucose. salt-wasting nephropathy (renal failure). usually glucose. multiple myeloma). Normal renal. * First step in determining why a patient is hyponatremic is determining the osmolality. * Pseudo-hyponatremia can occur also with normal osmolality. In this case. Thus adjusted sodium is 136. What test will show the cause of the patient’s hyponatremia? Answer is serum lipids (triglycerides).8. showing hyponatremia (diluted) and hyperglycemia (from the dextrose). there is less space for the sodium and water component of blood. High volume status assessed with edema. -------------------------------------------------------------------------------------------------------------------------------------------Electrolyte Disorders: Hyponatremia * Hyponatremia is arguably the most common of the sodium and potassium abnormalities seen in the hospital. Renal loss (urine Na+ > 10) due to diuretics. Extrarenal loss (urine Na+ < 10) due to GI loss from vomiting. symptoms include seizures. * Causes of SIADH include lung disease. coma. * Patient presents with diabetes. glucocorticoid deficiency. diuretics. neoplasm-related (most common is small/oat cell in the lung). water intoxication (> 12-20L/day. lab shows osmolality is low. drug side effect. so the patient’s volume status. Blood osm is low/dilute.2 in sodium drop. sodium is 128. * Hyponatremia algorithm: once we rule out high osmolality and normal osmolality.2 (normal). So again. think acute tubular necrosis (ATN). the patient has fluid loss with causes including GI. SIADH. * Hyponatremia with high osmolality caused by increase solute in the blood. Fluid shifted into blood dilutes Na+ level. tube drainage. With severe or rapid change. hypoaldosteronism. including cirrhosis and congestive heart failure. Labs show glucose of 402.8 difference for sodium. normal volume states. DO NOT DISTRIBUTE . so 3*1. and burns. hyper-proteinemia was ruled out. sweat. * Causes of hyponatremia include pseudo-hyponatremia. When protein/lipid increase. * If the ECF is high (hypervolemia). so sodium is actually 129 adjusted. symptoms include headache and confusion. sweat. sodium of 131. Emergency treatment is hypertonic saline (3% or 5%). treat the glucose. kidney. Say glucose is 342 and sodium is 126. Osmolality can be determined by direct measurement (best) or by calculation (osmolality = 2*Na + glucose/18 + BUN/2. and hyponatremia with low osmolality (true hypoglycemia. * With normal osmolality pseudo-hyponatremia. * Hyponatremia mild or gradual change the patient will most likely be asymptomatic. adrenal. or due to skin loss from burns. think pre-renal give fluids. the next step is to measure the extracellular fluid volume. or a simpler but less perfect method is 2*Na + 10). * SIADH has urine osmolality inappropriately high in the face of hyponatremia with low serum osmolality. glucose is 142. diarrhea. bowel obstruction. * Low osmolality with hypovolemia. So in hyperglycemia. So the glucose does not explain all of the drop in the sodium.Study Notes – Internal Medicine James Lamberg 28Jul2010 syndrome. If the ECF is normal (euvolemia).6 is 4. Normal blood osmolality is between 280 and 300. the patient’s sodium is not truly low thus do not treat the sodium. Does the glucose explain the level of hyponatremia? Here. that glucose accounts for about 3. and hepatic failure or cirrhosis. hyponatremia with normal osmolality (high lipids or protein). * Hyponatremia with high osmolality (hyperglycemia). low volume status assessed with tachycardia and orthostatic hypotension. brain disease. So hyper-triglyceridemia is next. Causes osmotic fluid shift from intracellular space into the blood. volume depletion.

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

ABG also gives O2 and PO2. and sleep apnea. O2 sat typically in mid-90s. has tightness in her throat and chest. * 67yo woman with HTN is on HCTZ. never overcompensation. HCO3 unchanged because not enough time. low chloride. decreased PCO2. Hemolysis of cells causes the potassium to be released from the cells. an inability to blow off CO2. Pickwickian (obesity hypoventilation syndrome). acute pulmonary disorder (pulmonary embolism. such as an error in the hospital with excessive potassium administration. A pH < 7. ACE-inhibitors). Patients needs treatment if ECG changes present. ABG shows 7. should be above 90% normally. also with bicarbonate as the alkalosis drives potassium into cells. * Respiratory acidosis caused by hypoventilation (acute or chronic). occurs in acidosis (H+ into cells. anxiety (acute pain. * 24yo female comes to the ED feeling like she is suffocating. which can vary by the altitude you live at. She presents for a routine checkup. could be renal failure.52/25/PO2/27/99%. PCO2 at 25 is low. Common causes of H+ loss include prolonged vomiting or other GI loss and diuretics (H+ and Cl. Drives down the PCO2 with no time for metabolic compensation. or asthma. early aspirin toxicity. Common causes of HCO3 gain include NaBicarb ingestion (multiple antacid pills) and milk-alkali syndrome (CaCO3). Exam shows orthostatic hypotension. Chronic causes include COPD. and rarely familial periodic paralysis. Acute causes include narcotics. potassium sparing diuretics. How will you treat this? * Treatment should start with protection of the heart. rhabdomyolysis.5 and potassium is 6. Electrolytes show low potassium. increased HCO3. * Respiratory alkalosis will have increased pH.4 +/. HCO3 rises with time to compensate almost back to a normal pH. * What if the patient above had an O2 sat of 76%? This is not acute anxiety or panic attack. Could be a patient on birth control pills with acute pulmonary embolism.28 - . DO NOT DISTRIBUTE . Potassium is one of the chemicals used for lethal injection because it causes heart block and asystole. pneumonia). where you can determine if this is acidosis or alkalosis. Next step is to lower the potassium level by driving potassium into the cells. leading to falsely high potassium levels. Hypoaldosteronism and adrenal insufficiency are other cause. * 67yo woman with diabetes and hypertension is on glyburide and ACE inhibitor. This is a lung problem. K+ out). -------------------------------------------------------------------------------------------------------------------------------------------Acid-Base Disorders * A normal blood pH is 7. likely due to the hyperventilation. * Metabolic alkalosis has increased pH. So PCO2 of 47 is high. You get HCO3 (normal 20-28). Why did her potassium become high? There are a number of reasons include the ACE-I. Pseudo-hyperkalemia can occur as an artifact from venipuncture or cell lysis from shaking the blood tubes. * Symptoms include weakness that increases with potassium level. * Metabolic alkalosis is either a loss of H+ or a gain of HCO3. sudden cardiac conduction defects preceded by classic ECG changes (talk pointed peaked T-waves). * Arterial blood gas (ABG) gives you pH. This is done with cation-exchange resin (kayexalate) or dialysis if renal failure. IV replacement maximum is 10mEq/hour via peripheral IV or 20mEq/hour via central line.interchange). Either way it is a lung problem.43 is alkalosis. replace orally. and if sustained the kidneys will retain HCO3 in an attempt to lessen the acidosis. these changes are rapid. low sodium. * Respiratory acidosis has decreased pH. Whenever possible. You get PCO2 (normal 35-45) and should determine respiratory rate/volume. An excessive rate causes cardiac conduction defects including heart block and/or asystole. Last step is to get rid of the potassium from the body. these changes are slower (2-5 days). This is uncommon except in conjunction with certain medications (e. RR is 36. with compensatory slowing of respiratory rate and increase in PCO2. This is done with glucose and insulin. * Metabolic alkalosis is a chronic process. This is respiratory alkalosis. The PCO2 being high is respiratory compensation.0. complains of fatigue. Another causes is deceased renal excretion from renal failure or medications like spironolactone and ACE-Is. acute COPD. This can also occur if blood is drawn proximal to a running IV drip that contains potassium.42/47/PO2/33/97%. with bicarbonate working as a metabolic buffer. Labs reveal creatinine increased to 4. HCO3 unchanged because not enough time. She appears anxious. They still have potassium in their body but it is no longer in the circulation where it would induce cardiac arrhythmia. ABG is 7.37 is acidosis and pH > 7.6. respiratory rate slows to raise PCO2 thereby increasing pH almost back to a normal value. obesity. * Respiratory alkalosis is caused by hyperventilation.03. This is metabolic alkalosis defined by high pH and high HCO3.g. and HCO3 of 33 is high. Hyperventilation lowers PCO2 and breath holding or shallow respirations will increase PCO2. Movement of potassium from cells into the blood can cause hyperkalemia. -------------------------------------------------------------------------------------------------------------------------------------------Electrolyte Disorders: Hyperkalemia * Causes include increased potassium intake.Study Notes – Internal Medicine James Lamberg 28Jul2010 * Treatment of hypokalemia is done by replacing potassium. pain attack). Give CaCl or Ca++ gluconate infusion. increased PCO2.

Diagnosed by seeing bicarbonate lost in urine in the face of acidic blood. so 8-14. lactic acidosis.e. * Anion gap > 14 caused by overproduction or under-excretion of an acid other than HCl. urine would be inappropriately high pH in RTA. Diagnosed by high urine sodium with salt restriction (salt restriction test). Arizona.29/29/PO2/17/97%. lactic acidosis. inability to excrete acid. the body does not overcompensate. iron/INH. * Anion gap < 14 (normal) usually caused by HCO3 loss in GI tract or urine or inability to excrete acid in urine. This is metabolic acidosis as bicarb is low. * Oxalate. Inability to acidify urine. idiopathic hypercalciuria. * Ketoacidosis is due to overproduction of ketone bodies. ABG shows 7. uremia. Chloride levels are unaffected “normochloremic.3. urinary pH typically > 5. diabetic. others). * Type 4 RTA occurs due to hypoaldosteronism. ABG shows 7.37/5/PO2/34/90%. How do we know this is not primary metabolic alkalosis (i. * Five kinds of stones: calcium oxalate (most common). uric acid. which should be acidic (< 5. amphotericin B. metastatic cancer). hyperoxaluria (fat malabsorption as fat binds to calcium. diabetic ketoacidosis. * Oxalate stones account for about 70%. Pupils small. Urate may not be seen on plain x-ray. Cl 113. Normal anion gap acidosis is excess HCl or loss of HCO3. Is this metabolic or respiratory? Answer is metabolic acidosis.g. * Metabolic acidosis has decreased pH. renal failure (uremia). PCO2 being low is compensatory. inc HCO3 with inc PCO2 compensating)? We know this because the pH of 7. sickle cell. Wilson disease. * MUDPILES: methanol. Is this acidosis or alkalosis? Answer is acidosis. phosphate about 10%.29 - . magnesium/ammonium/phosphate (“triple phosphate” or struvite). cysteine (rare). HCO3 18. paraldehyde/phenformin. vitamin D deficiency.37 is not alkalosis. DO NOT DISTRIBUTE . * Type 2 RTA occurs in the proximal tubules of the kidney. Seen in myeloma. are radiolucent and may not be seen by CT or other x-ray. Intoxication causes addition of non-HCl acids. and increased respiratory rate as compensation in an effort to blow off PCO2 thereby increased pH almost back to normal. * Type 1 RTA occurs in distal tubules of the kidney. or intoxication (ethylene glycol. lithium. What is the most likely cause of the this patient’s normal anion gap metabolic acidosis? Most likely diarrhea. * 72yo woman has COPD worsening over weeks. has altered mental status. * Metabolic acidosis is a relative increase in the quantity of acid. Lytes are Na 140. salicyclates. urate about 5%. body is breathing fast to bring down PCO2. struvite about 5-10%. decreased HCO3. tissue breakdown (e. hyperparathyroidism. with causes including addition of acid. * Metabolic acidosis is the most complicated of the group. K 2. and struvite have calcium and are radio-opaque. destructive bone disease (myeloma. Comes to the ED because she is becoming gradually SOB.31/30/PO2/17. vitamin C excess. Treatment is volume restriction.3). so normal anion gap (11 +/. Occurs with aldosterone or adrenal insufficiency and diabetes.g. calcium phosphate. fludrocortisone. ethylene glycol. Anion gap is normally 11 +/. Anion gap = (Na + K) – (Cl + HCO3). * Must determine which type of metabolic acidosis. Treatment is oral bicarbonate. This is a narcotic overdose with respiratory acidosis due to hypoventilation. alkaline urine favors crystallization of struvite and can result in large stones (staghorn calculi). methanol wood alcohol. * 17yo with diabetes has not been taking his insulin. What would be the best test to distinguish diarrhea from RTA? Answer is urine pH. cysteine rare. * High anion gap acidosis is an excess of non-HCl acid. vitamin D intoxication). What is the anion gap? Gap is 12. As compensation. and loss of base (HCO3). Common causes are diarrhea and renal tubular acidosis (RTA). Diagnosed by giving acid load/challenge test and still can’t acidify urine. leaving oxalate for excessive absorption). salicylate. ABG shows 7. more common in desert southwest (e. Respiratory rate is 7. Nevada). * Main causes of calcium oxalate/phosphate stones include increased calcium absorption (sarcoid. starvation). either high-anion gap (anion gap) or normal anion gap (nonanion gap). Needle tracks on arms. hematologic malignancies).28/56/PO2/28/84%. Could be RTA. * 72yo man has 4 days of diarrhea and presents to ED with weakness. -------------------------------------------------------------------------------------------------------------------------------------------Kidney Stones (Nephrolithiasis) * Urolithiasis occurs in 1-5% of the US population. Seen in kidney stones. occurs rapidly. * Renal tubular acidosis key clue is the inability to acidify urine. Inability to absorb bicarbonate until levels very low.9.4 or even overtly alkaline.Study Notes – Internal Medicine James Lamberg 28Jul2010 * 27yo man found unconscious on the street. klebsiella. * Main causes of uric acid stones include gout. Treatment is mineralocorticoid replacement. Lactic acidosis is due to overproduction of lactic acid. so likely a CO2 retainer with the COPD. ABG shows 7. phosphate. * Main causes of struvite stones include infection with urea-splitting bacteria (proteus most common. Her PCO2 is high. Fanconi syndrome.” There are four major causes: ketoacidosis (alcoholic. pseudomonas).4) in the presence of blood acidemia. Renal failure causes inability to excrete organic (non-HCl) acids. Presents with hyperkalemia.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

given oral. go for sigmoidoscopy. difficile. paramedic. colonic (left sided abdominal tenderness). Stop antibiotics in these cases. quinidine. difficile causes a secretory diarrhea. colchicine. Bacteria can ferment the lactose so patient can get a lot of gas and discomfort as well. so the small intestine tries to dilute it by adding water into the lumen of the small bowel. so gap of 76mosm of something that does not belong there. 3 exploratory laparotomy operations.57 - . * Direct way to make the diagnosis would be to put a sigmoidoscope in the patient and look for pseudomembranes. etc.Study Notes – Internal Medicine James Lamberg 28Jul2010 calcitonin. gold salts for rheumatoid disease. * Young female patient has supposed secretory diarrhea. * If patient cannot tolerate metronidazole (e. if cytotoxic then we know it is coming from C. There are also strains of VRE (vancomycin-resistant enterococcus) “superbugs” so metronidazole is first-line. Add stool to plate. diff can start to flourish. so this is an osmotic diarrhea. appendectomy. If very sick patient. * Most C. What is your next step in the evaluation of this patient? * Top of the differential list should be pseudomembranous colitis (C. antibiotics as a side-effect. gut tries to dilute non-absorbable lactose. difficile are being in a hospitalized/nursing home setting. * Osmotic diarrhea means there is an osmolar substance that is not absorbed in the small intestine. * Say you measure 2*(Na + K) as 274 and osmolarity is 350.g.g. difficile make pseudomembranes. usually non-bloody. He is treated for 7 days with IV cefazolin with dramatic improvement in his symptoms. difficile colitis includes clindamycin (most likely). but not all patients with C. patient is taking laxatives. Patient in the hospital is likely nosocomial or medications. * Most common osmotic agent is lactose. * Stool Osmolar Gap is a calculation you will probably only see on the boards. Enterocytes have villi and microvilli with lactase enzyme. He returns home and does fine until one week later when he has 6 watery green bowel movements a day and a low grade fever. do a toxin assay. IV metronidazole gets into blood stream but not really to lumen of the gut. He has had diarrhea for the past 5 days. salmonella. * Ways to get C. and even that is not perfect because the spores are so sticky. * Treatment is metronidazole first-line. * Everyone with pseudomembranes on exam has C. PO (oral) is very effective. difficile patients do not have sky-high white counts. but if it is present it points you to C. * Patient do not develop shigella. nurse). * Pseudomembranous colitis associated with a very high white count (e. difficile so hand-washing with soap and running water is required. like cholecystectomy for vague symptoms. To get stool osmolality 2*(Na + K) so 274 here. You’ve done all the studies and hormone assays but found nothing. Next step is vancomycin. even if you’re a gastroenterologist. Patient may have connection to the medical field (works in drug store. Ischemic Colitis * 72yo man complains of LLQ pain for the past few days. difficile does not grow in the gut but when you wipe out the normal flora with antibiotics the C. Exam shows vague mile left mid-abdominal pain. So not likely osmotic diarrhea. Patient may have multiple operations that they don’t have good reason for. receiving antibiotics. Normally C. so look at medication list for antibiotics. Medication causes include magnesiumcontaining drugs. * In clinical practice. milk sugar. Think factitious diarrhea. diff lives in the lumen of the gut so you want to clear it from the lumen of the gut. Say it is 275. which are yellow exudative plaques on the colon. This appearance does not look like anything else so you can tell the patient right there that they have pseudomembranous colitis.000). Pseudomembranous Colitis * 59yo construction worker is admitted to the hospital for treatment of cellulitis that developed after dropping a steel beam on his leg. With lactase deficiency. terrible neuropathy) use vancomycin. * Causes of C. they don’t want to wait for a few days they want to know now so get your sigmoidoscope and get moving. stools bloody DO NOT DISTRIBUTE . difficile colitis). * Antibiotic-associated colitis (non-pseudomembranous) is diarrhea associated with the change in flora that occurs with antibiotic use. * C. * 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. WBC of 30-50. you can differentiate osmotic from secretory diarrhea from clinical presentation and initial laboratory testing. close to 274. Vancomycin is more expensive than metronidazole. spectrum from well with mild diarrhea to very toxic-appearing with high fevers. campylobacter in the hospital. difficile. can wait for toxin assay. or being exposed to diarrhea (nosocomial infection). C. There are also strains of vancomycin-resistant staphylococcus. In a negative sigmoidoscopy. probably secretory. So besides the Na+ and K+ there is nothing else that has osmolar properties in the stool. * Now measure osmolality directly for the stool. You may get called to the ICU for a very sick patient who has been on many antibiotics. Also cephalosporins or penicillins because we use those medications more than clindamycin. difficile. Alcohol-based hand sanitizers do not remove C. If not very sick.

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

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

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

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

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

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

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

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

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

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

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

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

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

the other three glands shrink due to negative feedback with calcium. For every drop in albumin by a single point there is a drop in calcium of 0. then calcitonin (immediate action. * Sarcoidosis can cause hypercalcemia. Treatment is usually not necessary. * A patient with nephrotic syndrome would have a lower total calcium. Say nephrotic patient is 2mg/dL albumin and total calcium level is 6. A patient who got exploratory surgery around the neck area could have had damage to parathyroid gland circulation. this is called hungry bone syndrome. * To distinguish in a hypercalcemia patients between primary hyperparathyroidism and hypercalcemia of malignancy. * Treatment is surgery for definitive treatment. hydrochlorothiazide retains calcium. * Hypercalcemia associated with cancer is usually severe. So sarcoid patients develop hypervitaminosis D in the summertime or when they go to sunny areas. Treatment here is IV calcium with ECG monitoring for QT abnormalities. make sure to account for low albumin states. this may be due to a gastrin producing pancreatic tumor (Zollinger-Ellison) with parathyroid tumor. * Mild hypercalcemia would be bone pain. So 6. which activates the osteoclast. Lab would be low phosphate. pituitary tumors. you order PTH level. * Familial hypocalciuric hypercalcemia is a benign disorder. but their ionized calcium would remain the same. * Most of vitamin D is absorbed in the summertime due to sunlight activation. So PTH-like substance may not be picked up by parathyroid hormone levels. In 15-20% of cases there is four gland hyperplasia or parathyroid cancer. * Furosemide and diuretics can be seen in hypercalcemia protocols because furosemide gets rid of calcium. it should be done in all patients with symptomatic hyperparathyroidism such as kidney stones. polydipsia. * Most blood assays only check for parathyroid hormone that is intrinsic. so hypervitaminosis D. Fluids is the cornerstone of treatment for hypercalcemia. then watching the serum calcium go up and down. * With one gland hyperplasia. so that is a case when you could give calcitonin at the same time as a bisphosphonate. DO NOT DISTRIBUTE . * Hypercalcemia of immobilization is also benign. * Older individual with mild asymptomatic hyperparathyroidism may be watched.Study Notes – Internal Medicine James Lamberg 28Jul2010 there is a single adenoma. where granulomas occur mainly in the lung but can occur anywhere. With vitamin D deficiency and in some stages of chronic renal failure the parathyroid hormone becomes ineffective. you have three glands that are not working well.8 factor = +1. They will have an elevated calcium level and it is not likely cancer or hyperparathyroidism. What is this patient’s real total calcium? Answer is (4mg/dL . giving diuretics if calcium is high or if kidney stones occur uncommon. * Normal albumin is 4mg/dL. putting one in the arm. Ionized calcium is the part that affects neuromuscular irritability.8.5. and parathyroid tumors. PTH level would be elevated only in primary hyperparathyroidism. Hypocalcemia after surgery for primary hyperparathyroidism is due to calcium going to bone and nothing left to stabilize the calcium. These are breakdown of bone.6. These patients hardly ever have symptoms. After surgery. * Fibrosa cystica (brown tumors) develops in the bone due to the constant osteoclast activation resulting in cyst formation. On the other hand.71 - . * With hypocalcemia. Severe hypercalcemia occurs with > 15mg/dL and is a medical emergency. polyuria. Example is squamous cell lung cancer or esophageal cancer.1 total calcium. Furosemide does not do much to the calcium level. so majority is protein bound. If calcium is still high. Hypocalcemia * Whenever you see hypocalcemia. it is given because the mainstay of treatment is fluids and we do not want to cause fluid overload in an elderly patient. This is the cause of the hypercalcemia (and more phosphorus too). wears off after 48hrs) or bisphosphonates (long acting) like pamidronate. Treat hypercalcemia with fluids (normal saline) primarily.6 = 8. Hypercalcemia causes shortened QT. It is a chronic granulomatous disease. Patient has hypercalcemia with severe peptic ulcer disease and diarrhea. So patient goes from hypercalcemia to hypocalcemia. * Hypocalcemia prolongs the QT interval. This would be a nursing home patient who is in bed most of the time. Watch these patients closely in a telemetry unit and monitor calcium levels for a couple of days. osteitis fibrosa cystica. The other mechanism is through production of PTH-like molecule. only give furosemide if evidence of overload. think about hypoparathyroidism. it grows focally. When we measure calcium in serum we get total calcium and 40% of this is ionized. abdominal pain. no need for medications or further testing. Hypercalcemia of Malignancy * Hypercalcemia of malignancy can occur through multiple metastases to bones. Diffuse granulomas seem to activate vitamin D. Do not write for IVF and furosemide at the same time here. * Four gland hyperplasia requires removing all four glands. such as multiple myeloma.2mg/dL) = 2 * 0. Squamous cell cancer does not metastasize much. Treatment is just to monitor the patient.5 + 1. * Primary hyperparathyroidism associated with MEN-I (the 3 Ps): pancreatic tumors.

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

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

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

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

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

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

Hg A is two alpha chains plus two beta chains. Hyperplasia (e. * To have AML. If the smear is normal. So one little mL contains all the iron you need for a day. Four gene deletion patients are dead. What do you do first to establish a diagnosis? Answer is peripheral smear. Alcohol can also cause dementia. Maximum absorbable is 3-4mg/day. medications (e. it just means tell the patient to avoid having sex with people who has the same genetic problems that they have (e. * Thalassemia anemia: normal iron studies. colon polyps. low TIBC. thus increased A2 and F. * Treatment of thalassemia minor (thalassemia trait) is do nothing. folate deficiency. * Left ventricle cannot distinguish between anemia (decreased oxygen delivery). These will all look hypochromic and microcytic on peripheral smear. Microcytic Anemia * Iron deficiency anemia is usually from blood loss. Who cares though. Macrocytic Anemia * 72yo alcoholic man is brought to you by his son because the man is having memory loss and some numbness and tingling of the feet.g. So in alpha thalassemia there are no beta chains. cardiomyopathy. RDW will be increased because the newer cells are smaller. which helps you determine the etiology. 5-6mg/day when pregnant. You only need 1mg/day of iron when not menstruating. family planning). * Next step in management is iron studies. Yep. iron running out. * Anemia of chronic disease: high ferritin. sideroblastic. * Stroke is also not the cause of death in anemia.78 - . zidovudine.g. What is the next step? Answer is look at cell size (MCV). so treatment with vitamin B6 can help them. * Sideroblastic anemia: high iron (only microcytic anemia with a high circulating iron level). Most sensitive test is bone marrow looking for stainable iron stores. peripheral neuropathy. genetic counseling. refractory anemia with ringed sideroblasts. you can live by being stupid and in love but not intelligent with no love. * Microcytic anemia (TICS): thalassemia. You can live without your brain functioning but cannot live without your heart functioning. If the smear is abnormal showing DO NOT DISTRIBUTE . methotrexate. myopathy. Unit packed cells of 350mL is enough iron for a year. alcohol. Reticulocytes are usually larger. high TIBC. chronic myelomonocytic anemia. Hg F is two alpha chains plus two gamma chains.g.g. There are about 5mL in a teaspoon and 15mL in a tablespoon. coronary artery stenosis (decreased oxygen delivery). skin. but the new cells will be more deficient than the old cells. Hct is 28. Myelodysplasia (MDS) is premalignant for leukemia (AML). high is macrocytic. MCV is 110 (normal 80-100). pancreas. Hereditary deficiency in pyridoxine metabolisms. Genetic counseling does not mean do all the karyotype testing. cervix) is premalignant. these are myelodysplasia with a certain percentage of blasts. thus is the most common drug cause of macrocytic anemia. blood loss. * Iron deficiency anemia: low ferritin (most specific).Study Notes – Internal Medicine James Lamberg 28Jul2010 causes are usually managed. * Latest and greatest treatment for iron deficiency anemia is iron. but this is not the first test. say you get hemochromatosis from iron overload with iron deposits in organs (liver. Associated with lead poisoning. * Normocytic anemia: hemolysis. and refractory anemia with excessive blasts are all the same disease. There is no real mechanism to get rid of excess iron. * Dysplasia (e. * Unit packed RBCs has 1mg/mL of iron. iron deficiency anemia. Half the volume of stool is cells. * Most normal iron loss is through the GI tract. you need 30% blasts. Total iron binding capacity (TIBC) is unoccupied sites. If low it is microcytic. heart. We cannot treat this form of hemochromatosis (secondary to thalassemia major) with phlebotomy. * Thalassemia major requires a unit of cells every 2-4 weeks. Hg A2 is two alpha chains plus two delta chains. these symptoms are from alcohol. it comes down to hypochromic microcytic anemia with normal iron studies. Single gene deletion patients are normal so not likely to be seen in clinic. * Mean corpuscular volume (MCV) tells you the size of the RBCs. so you will continue to have bowel movements even if you do not eat. 23mg/day when menstruating. fibrocystic breasts. Electrophoresis tells you what type of thalassemia. testicles). benign prostatic hypertrophy) is not premalignant. * Hematocrit (Hct) is found to be low. Two gene deletion is mild anemia and three gene deletion is moderate anemia. * Alcohol directly suppresses bone marrow. Refractory anemia. * Ferritin is the storage form of iron. and carbon monoxide poisoning (decreased oxygen delivery). or normocytic. * Latest and greatest treatment for anemia of chronic disease is to treat the chronic disease. You could treat hereditary hemochromatosis or polycythemia vera with phlebotomy. * Macrocytic anemia: B12 deficiency. * Treatment of iron overload in thalassemia major is deferoxamine. liver disease (liver cannot metabolize fats/lipids and they stick to the RBCs). * Treatment for thalassemia major is blood transfusion every few weeks. mercaptopurine). chronic disease anemia.

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

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

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

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

000) because bleeding time will always be abnormal. If you have platelets and ristocetin with vWF present they will stick. * TTP is associated with renal failure and hemolysis. then you might give cryoprecipitate. * Factor VIII antigen (vWF) travels bound to the factor VIII coagulant portion (hemophilia). give factor VIII replacements because it comes with some von Willebrand factor (vWF). This rapidly brings up the vWF level. What is the treatment? Steroids. * First thing to do with a bleeding question is determine the nature of the bleeding before you look at the labs. Excision biopsy shows Reed-Sternberg cells. mucosa. you could look at the empty beer bottles (D-dimer) or the bottle caps that were split off (fibrin split products). Adriamycin gives cardiac toxicity. gums. What is the next step in management with the assumption of von Willebrand? Answer is bleeding time (prolonged). * Desmopressin releases sub-endothelial stores of vWF. * After the initial clot is formed via vWF with platelets and endothelium. * DIC has low platelets. Vincristine and vinblastine causes peripheral neuropathy. factor-type bleeding.Study Notes – Internal Medicine James Lamberg 28Jul2010 * Treatment of non-Hodgkin lymphoma is CHOP. where it is made and stored. If that doesn’t work. platelet-type bleeding. * They tell you the spleen is normal to rule-out splenic sequestration. Cyclophosphamide causes hemorrhagic cystitis. so it is not unusual to see prolonged PTT in von Willebrand disease. Fibrin is broken to D-dimers (fibrin parts) by plasmin. increased PTT. Testicles are more vulnerable to this effect. So do bleeding time when you see platelet type bleeding with a normal platelet count. skin. Factor VIII and vWF sit in the endothelial lining. This is the ristocetin test (artificial endothelial surface). What is the most likely diagnosis? This is platelet-type bleeding with a normal platelet count. the platelets do not stick to ristocetin. * Vitamin K deficiency: prolonged PT. so in the 26yo patient so most likely von Willebrand since it is the most common hereditary coagulopathy. von Willebrand disease. * It is not vitamin K deficiency because PT is normal. platelet count low. This is idiopathic thrombocytopenic purpura (ITP). fibrin come in and cross-links the clot. night sweats. * Glanzmann thrombasthenia and Bernard-Soulier syndrome are rare. * In order for platelet and endothelium to stick to each other they need vWF. If vWF is not there. * Megakaryocytes are precursors to platelets. hematoma in muscle) or platelet bleeding (superficial like epistaxis. * Radiation of local disease results in a cure 90% of the time. leading to good clotting. platelet count of 217. 1% a year develop AML. normal platelets. IX) are clean because they are no longer pooled blood products. MOPP. thus it is not used much. Factor XIII helps preserve the clot. Then get a von Willebrand factor level. If DDAVP does not work. so increased in ITP. It is not hemophilia because she is a woman. Hepatitis B vaccine is made this way too. PTT normal. Then you take a razor blade and cut the patient. factor-type bleeding. * Busulfan and bleomycin cause pulmonary fibrosis. * If you wanted to know how many beers someone drank. Bleeding time is a test of platelet function. weight loss. so do not do a bleeding time if the platelet count is low (< 50. To see if there is functional vWF. Tissue plasminogen activating factor (tPA) so that the plasminogen turns into plasmin and then the plasmin chops up the fibrin linked clot. Then you time the bleeding. normal PTT.83 - . you need an artificial endothelial surface. * Treatment of von Willebrand disease is desmopressin (DDAVP). PTT is prolonged at 52s. They are made with E. normal platelets. Cryoprecipitate is pooled blood products and can transmit disease. normal platelets. Pelvic CT scan is positive for lymph nodes consistent with lymphoma. fever. * Von Willebrand disease: normal PT. Fibrin split products gets split off from fibrinogen to activate it to fibrin. ABCD) is sterility in 95% of patients. What would you do next in the management of this patient? Stage is IIIb so do chemotherapy with ABVD/MOPP. but enough so the artery is open. * 32yo woman with a neck mass. Her prothrombin time is normal at 11s. * Factor replacements (VIII. PT is normal. vagina)? * Hemophilia: normal PT. 1% will develop aplastic anemia. * How do you do bleeding time? You put on a BP cuff to occlude the veins of the arm.000. * Say you have platelet-type bleeding with normal platelet count. prolonged/normla PTT. Bleeding Disorders * 26yo woman presents with epistaxis and petechiae. coli and recombinant technology. What is the next test for diagnosis? Answer is antiplatelet antibody test. but you need a bone marrow biopsy to see these. increased PT. * 26yo with platelet-type bleeding. prolonged PTT. Is this factor related bleeding (deep like hemarthrosis in joint. DO NOT DISTRIBUTE . The spleen is not enlarged on exam. Cisplatin causes nephrotoxicity and ototoxicity. * Most common side effect of chemotherapy (CHOP. Why don’t we just chemo everyone? Side effects. * Treatment of Hodgkin lymphoma is ABVD/MOPP. with factor-type and platelet-type bleeding.

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

Study Notes – Internal Medicine

James Lamberg

28Jul2010

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

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Study Notes – Internal Medicine

James Lamberg

28Jul2010

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

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Study Notes – Internal Medicine

James Lamberg

28Jul2010

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

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

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

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

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

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

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

eptifibatide. showing complete heart block. the management is the same for unstable angina and MI. subarachnoid hemorrhage. Overall reduction in mortality with thrombolytics is 25%. Which of the following is the most likely diagnosis? * Right coronary artery feeds the right ventricle. * All patients who get angioplasty also get a stent to keep the vessel open. * Most common cause of death immediately post-MI is arrhythmias. but troponins are even more specific (99.9%). During times of exertion. * Also. epidural hematoma. No hypotension because the blood pressure cuff did not exist then. causing rales. This is not the right answer though. CK-MB (97-99%) is specific. They saw lightheadedness. He has melena. but the heart would beat faster to compensate (here the patient has bradycardia). * For MI. cannon a waves. The pain goes to his neck and arm. do a pericardiocentesis or a cardiac window then repair the hole. thrombolytics. thus you would not give these in an acutely bleeding patient. * CK-MB and troponins do not begin to arise for 4 hours. bradycardia. * LDH is no longer used in the diagnosis of myocardial infarction. described first in 1826 by Stokes and in 1846 by Adams near the University of Dublin. * Transvenous pacing cannot be setup fast enough and requires an invasive procedure. If they do not change management. lasting for the past hour. petechiae. you will still give aspirin. * What is the best initial management? Atropine. they didn’t have ECG back then. Uterus can still make a little CK-MB but no troponins. Prophylactic lidocaine suppresses those arrhythmias. because streptokinase can produce antibodies resulting in anaphylaxis. 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. and tirofiban. RV infarct and cardiac tamponade could give clear lungs. * 64yo man with a history of hypertension and hyperlipidemia comes to the ED with chest pain. syncope. Atheromatous plaque gets covered by a little later of endothelium. a chest that is clear to auscultation. Lidocaine also causes arrhythmias. allowing the sympathetics to work without inhibition and thus speeds up the impulses through the AV node. 40% of inferior wall MIs also have RV infarcts. but it also makes all the chest muscles contract. The problem is when you remove the catheter the plaque can bulge back out.Study Notes – Internal Medicine James Lamberg 28Jul2010 * Beside thrombolytics or heparin. It is like a car that has an accelerator (sympathetics) and brakes (parasympathetics). These are antiplatelet drugs and can make you bleed. * Cardiogenic shock would give rales. may need to go in and emergently replace the valve. * When a patient comes in with chest pain and ECG abnormalities. * Complications of an MI can all cause hypotension and hypotension can cause confusion. * Efficacy is the same with tPA (tissue plasminogen activator) and streptokinase. Angioplasty is when a catheter is placed through the partially occluded artery then a balloon is expanded to open the vessel. pulse is 40. heavy periods. Patient’s blood pressure is 70/40. Heart exam reveals 3/6 murmur. ECG shows ST segment depression in V2-V4. * CK-MB last 1-2 days. * Myocardial wall rupture with cardiac tamponade would lead to hypotension and confusion. thrombolytics can be given up to 12 hours from the onset of chest pain (3 hours for stroke). * What is the best initial diagnostic test? ECG. * If cardiogenic shock and extension of the MI. but it doesn’t work that way. why order them? If the CK-MB is up with ST segment elevation. But no. DO NOT DISTRIBUTE . * Think about what it could be. Valve rupture would regurgitate into the lungs. The mortality benefit with thrombolytics is enormous in the first 1-2 hours. a subdural hematoma. up to a 50% reduction in mortality within the first hour. If CK-MB not up. Atropine cuts the brake lines for a while. * Glycoprotein IIb/IIIa inhibitors are abciximab. thrombolytics dissolves the clot then give heparin afterwards to keep it open. maybe it is just not up yet since they begin to rise at 4-6 hours and take 12-24 hours to reach peak. Thus you leave a meshwork stent “scaffolding” to keep it expanded. * If valve rupture. and inferior wall. LDH is not abnormal from 12-24 hours. This blocks the parasympathetic. do not wait around for enzyme changes. He received all the appropriate therapy. Nope. Use tPA if patient previously got streptokinase. This patient has a clear lung auscultation exam.94 - . has cannon a waves. Troponin I is the most sensitive and specific. We could go to sermons all day long to become saints. * If cardiac tamponade. * What about extension of the MI with cardiogenic shock? Not that either. beta blockers. * Answer is third degree complete AV heart block. so why not use lidocaine? Because it does not change the mortality. * Transcutaneous pacer makes the heart beat with capture. You are called by the nurse because “he is confused”. * Valve rupture with chordae tendineae rupture (after a week) could cause a murmur and hypotension. troponins last 1-2 weeks. AV node. Wait. Post Myocardial Infarction Management * 65yo man in the coronary care unit (CCU) after having an inferior wall myocardial infarction last night. may need emergency bypass surgery. Stethoscope invented shortly before by Laennec in France (1816). the plaque ruptures which causes a sudden clot to occlude the artery.

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

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

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

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

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

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

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

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