26182164 Study Notes Internal Medicine

(1)

Study Notes – Internal Medicine James Lamberg 01Feb2010

Textbooks

Textbooks: Cecil Essentials of Medicine, Hospital Medicine Secrets, First Aid for Medical Clerkship Introductory Guide

Introductory Guide : Primer to the Internal Medicine Clerkship, 2nd Edition, by Picchioni Common Problems in Internal Medicine

Common Problems in Internal Medicine

Cardiovascular: Acute Coronary Syndromes, Congestive H eart 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:

Procedures: NEJM Videos In Clinical Medicine: http://content.nejm.org/misc/videos.dtl How To Succeed In

How To Succeed In Clerkship – First Aid For The Clerkship – First Aid For The Medicine Clerkship (Stead, Stead, & Kaufman)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 _{your professional dress clothes unless it is discouraged (e.g. pediatrics).}: Regardless of what the attending wears. A short white coat should be worn over 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 understand or disagree with a treatment plan or diagnosis, do not “challenge.” In-stead, 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.

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) 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.

(2)

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)

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

* 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) 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 m antra: 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]/[atr ial 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.

(3)

4) Intervals: The [PR]/[QRS] intervals are [normal]/[shortened]/[widene d]: * 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/a trial] 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.

Top 100 Secrets –

Top 100 Secrets – Medical Secrets (4th, Zollo)Medical Secrets (4th, Zollo)

1) The treatment of severe sepsis syndrome should be based on efficient resuscitation, effect ive antimicrobial therapy, elimination of secondary infections, euglycemia, early targeted and specific drug therapy, and establishment of therapeutic goals.

2) Acute pulmonary embolism (PE) is a difficult diagnosis to establish despite newer advances in imaging; approximately 50% of cases are diagnosed post mortem.

3) In the approach to suspected PE, keep in mind the prudent use of key diagnostic tests: (1) rapid d-dimer by ELISA is an effective screening test; (2) chest CT can help detect most PEs; and (3) a negative Doppler venous ultrasound of the legs does not exclude the diagnosis of PE.

4) The most comm on etiologic agent implicated in acute bacterial meningitis in the U .S. is Streptococcus pneumoniae.

5) In the newly diagnosed HIV patient, in addition to routine adult immunizations, immunizations against pneumococcal pneumonia, influenza, and both hepatitis A and B are indicated.

6) Metabolic syndrome is diagnosed on the basis of abdominal obesity, hypertriglyceridemia, low HDL cholesterol levels, hypertension, and fasting hyperglycemia.

7) Pituitary tumors cause problems for patients by two main mechanisms: mass effect, which applies pressure to surrounding structures, and endocrine hyperfunction, which results in excessive secretion of a particular anterior pituitary hormone.

8) A key concept in evaluating patients with hyperfunctioning endocrine tumors is that biochemical diagnosis should always precede anatomic localization.

9) The best initial screening test for evaluation of thyroid status is the TSH, since it is the most sensitive measure of thyroid function in the majority of patients. The one exception is patients with pituitary/hypothalamic dysfunction, in whom TSH cannot reliably to assess thyroid function.

10) The most common presentation of hypogonadism is erectile dysfunction and decreased libido in men and amenorrhea and infertility in women.

11) All patients with coronary artery disease (CAD), CAD-equivalent diseases, or diabetes should be treated aggressively to reach the LDL-cholesterol target of 100 m g/dL.

(4)

12) Diabetics and patients with vascular disease should be treated with a statin lipid-lowering drug to prevent heart disease and stroke, regardless of the blood low-density lipoprotein (LDL) cholesterol level, age (from 40 to 79 years), or gender.

13) The goal blood pressure is < 130/80 mmHg in hypertensive subjects with diabetes mellitus and/or chronic kidney disease.

14) The single most life-saving treatment strategy in patients with acute ST-elevation myocardial infarction is to rapidly achieve complete reperfusion of the infarct-related artery by mechanical (balloon angioplasty or stenting) or pharmacologic means (thrombolysis).

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.

16) Noninvasive stress testing has the best predictive value for detecting CAD in patients with an intermediate (30-80%) 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, higher titers of complement-fixing antibodies suggest more extensive disease, and rising titers suggest worsening disease.

18) Patients who present with flaccid paralysis during the summer months should be evaluated for West Nile virus infection.

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.

20) Community-acquired methicillin-resistant Staphylococcus aureus that is susceptible to clindamycin but resistant to erythromycin should not be treated w ith clindamycin because of the possibility for induction of resistance. 21) In patients with disseminated candidiasis, IV catheters should be removed and ophthalmologic examinations performed to evaluate for the presence of retinal disease._{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.

23) Porcelain gallbladder is an incidental finding, more common in women who have gallstones. Because up to 50% of patients develop gallbladder carcinoma, prophylactic cholecystectomy is recommended.

24) Three liters of Coca-Cola administered via nasogastric lavage over a 12-hour period can dissolve gastric bezoars. It is thought that the cola acidifies the gastric contents and liberates carbon dioxide in the stomach, resulting

in the disintegration of phytobezoars.

25) Regardless of what is done, GI bleeding stops spontaneously in about 80% of patients.

26) Patients with hereditary nonpolyposis colorectal cancer syndrome have a higher-than-average risk of developing colon and gastric cancer.

27) About 90% of patients with primary sclerosing cholangitis have underlying ulcerative colitis, but less than 10% of all patients with ulcerative colitis have primary sclerosing cholangitis.

28) In patients with suspected perforation, the minimum amount of free air that can be detected on an upright chest x-ray is 12mL.

29) The three major openings in the diaphragm through which hernias may occur are the esophageal hiatus (most common), foramen of Bochdalex (3-5%, usually left-sided), and foramen of Morgagni (rare).

30) In a patient who has a malignancy involving the right hilum, look at the hand veins. If the veins in the hands are distended and do not collapse when the arms are lifted over the head, there is a high chance of superior vena cava obstruction.

31) In high-risk patients, the chance of developing breast cancer can be reduced by about 50% with the use of tamoxifen.

32) If a patient with lung cancer presents with hoarseness, look for vocal cord paralysis, 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, lung, or esophagus), especially if they continue to smoke and drink. 34) If a patient presents with hypercalcemia, look for a squamous cell cancer (lung, esophagus, head and neck, cervix, anus).

35) Up to 15% of breast cancers may not be detectable by mammogram. If the patient has a clinically suspicious lump, perform a biopsy.

(5)

37) In a diabetic patient with proteinuria, the presence of concomitant retinal disease suggests strongly (90% correlation) that the renal manifestations are due to diabetes.

38) Treatment of anemia of chronic renal failure by recombinant human erythropoietin is highly effective, but correction of iron deficiency and iron supplementation by oral or intravenous route is simpler, cheaper, and often by itself effective therapy.

39) In resistant hypertension, especially in younger (< 20 yr) or older (> 70 yr) patients, consider and rule out renovascular hypertension.

40) New onset of nephrotic proteinuria in an elderly patient warrants exclusion of an underlying malignancy. 41) The principal mechanism of bicarbonate reabsorption in the proximal tubule is through Na+-H+ exchanger (NHE3) activity.

42) D-lactic acidosis is characterized by increased serum anion gap, metabolic acidosis, and episodic encephalopathy in patients with short bowel syndrome.

43) Ethylne glycol (antifreeze) toxicity is characterized by high anion gap metabolic acidosis, neurotoxicity in the form of ataxia, seizures, and calcium oxalate crystals in the urine.

44) Bartter's syndrome is a disorder associated with normotensive hyperaldosteroni sm, secondary to juxtaglomerular hyperplasia, hypokalemic metabolic alkalosis, and severe renal potassium wasting.

45) Hyperkalemia is an important side effect of both ACE inhibitors and ARBs, but the problem is less frequent and smaller in magnitude with ARBs because of their less pronounced effects on aldosterone levels.

46) Hypochromic microcytic anemias are the most encountered anemias in hospitalized and ambulatory patients. 47) Both iron-deficiency anemia and anemia of chronic disease have a low transferrin saturation. In iron-deficien cy anemia, the TIBC is often increased, whereas anemia of chronic disease is marked by an unusually low TIBC. 48) The main clinical manifestations of sickle hemoglobinopathies are hemolytic anemia, chronic end-organ damage, periodic vaso-occlusive disease ("crises"), and hyposplenism.

49) The triad of thrombocytopenia, fragmentati on hemolysis, and fluctuating neurologic signs suggests thrombotic thrombocytopenic purpura (TTP), perhaps the most spectacular of the fragmentation syndromes.

50) The cytogenetic marker of chronic myelogenous leukemia is the 9:22 translocation, in which portions of the long arms of chromosomes 9 and 22 are exchanged, resulting in a shortened 22 or Philadelphia chromosome (Ph1). Some patients with acute lymphoblastic leukemia (ALL) also have 9:22 translocations (poor prognostic marker). 51) The classic cell seen in the lymph nodes of patients with Hodgkin's disease is the Reed-Sternberg (RS) cell, a large cell with two nuclei, each possessing a distinct nucleolus.

52) Secondary monoclonal gammopathy must be distinguished from the monoclonal gammopathy associated with multiple myeloma, benign monoclonal gammopathy of uncertain significance, solitary plasmacytoma, amyloidosis , lymphoma, and Waldenström's macroglobulinemia.

53) Deep venous thrombosis in a young person, a family history of thrombosis, thrombosis at unusual sites (such as the mesenteric vein), or recurrent thrombosis without precipitating factors suggests a hypercoagulable state.

54) Any condition that leads to V/Q mismatching can cause hypoxemia. Most pulmonary disorders are associated with some degree of V/Q mismatching. This is the most common cause of hypoxemia and is responsive to oxygen therapy.

55) Assuming that you are at sea level and breathing room air, an easy way to calculate the A-a difference is as follows: (150-40/0.8) - PaO2 measured by ABG.

56) Although the anterior segment of the upper lobes may be affected by TB, a lesion found only in the anterior segment suggests a diagnosis other than TB (e.g., malignancy).

57) Incidence of lung cancer now exceeds breast cancer in women. Women develop lung cancer at an earlier age and after fewer years of smoking.

58) Pleural fluid glucose < 30 mg/dL and pH < 7.30 suggest rheumatoid effusion, TB, lupus, or malignancy. 59) Mesothelioma, a pleural malignancy associated with asbestosis exposure, is not associated with tobacco use. 60) Early, aggressive intervention with disease-modifying antirheumatic drugs reduces the morbidity (deformity leading to reduced functionality and disability) and mortality associated with rheumatoid arthritis.

61) Antinuclear antibody (ANA) titers are not associated with activity of disease.

62) COX2 NSAIDs are no m ore efficacious than older standard NSAIDs but are significantly less toxi c. 63) A patient with low positive rheumatoid factor (RF) and arthralgia should be checked for hepatitis C, which can produce a low-grade synovitis and cryoglobulins (which in turn can produce a falsely positive RF).

64) Always check for Sjögren's antibodies (SSA/SSB) and phospholipid antibodies in a young woman with lupus before conception. Sjögren's antibodies increase the risk of neonatal lupus (rash, thrombocytopenia, heart block),

and phospholipid antibodies can significantly increase the risk for miscarriage, premature labor, or intrauterine growth delay.

(6)

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. 66) Intranasal steroids are the single most effective drug for treatment of allergic rhinitis. Decongestion with topical adrenergic agents may be needed initially to allow corticosteroids access to the deeper nasal mucosa.

67) The clinical manifestations of anaphylaxis include flushing, sense of foreboding, urticaria or angioedema, pruritus, hoarseness, stridor, bronchospasm, hypotension, tachycardia, nausea, vomiting, abdominal pain, diarrhea,

headache, and syncope.

68) ACE inhibitors are often-forgotten causes of angioedema and chronic cough.

69) Chronic urticaria may require treatment with a combination of both H1 and H2 antihistamines, reflecting the distribution of these receptors in the skin. Work-up for an allergic etiology is rarely informative.

70) Beta blockers should be avoided whenever possible in patients with asthma because they may accentuate the severity of anaphylaxis, prolong its cardiovascular and pulmonary manifestations, and greatly decrease the effectiveness of epinephrine and albuterol in reversing the life-threatening manifestations of anaphylaxis. 71) HIV infection is preventable and treatable but never curable.

72) If you are thinking of mononucleosis as a diagnosis, think about and test for HIV.

73) Adherence to anti-HIV therapy must be > 95% for a durable response. HIV treatment guidelines change frequently - always verify your information.

74) A person under care for HIV should not develop pneumocyotic pneumonia (PCP). It is entirely preventable. 75) There is a critical interaction between HIV and tuberculosis. If one infection is present, look for the other. 76) If you have diagnosed one sexually transmitted disease (STD), you must consider others, especially HIV. 77) Most back pain is not caused by a radiculopathy.

78) The most common cause of dizziness is benign paroxysmal positional vertigo.

79) The leading causes of death after a stroke are medical complications, not the stroke itself. 80) Heparin has no value in the acute treatment of strokes.

81) The sudden onset of a severe headache may indicate an intracranial hemorrhage. 82) Coma is usually caused by medical problems, not neurologic ones.

83) Elective surgery should be postponed for further evaluation if the patient has signs or symptoms of unstable or inadequately treated chronic disease.

84) Patients who have undergone coronary revascularizati on within 5 years of a proposed elective surgery and have no signs or symptoms of recurrent ischemia can usually undergo surgery without further evaluation.

85) Acute dyspnea in a patient who has had major surgery should raise the suspicion of pulmonary embolism, even if the patient has received prophylaxis.

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. In these cases the oral agent should be held at least several days in advance of the surgery.

87) Pacemakers and implanted cardioverters/defibrillat ors should be assessed both before and after surgery, radiation therapy, or lithotripsy.

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.

89) Strict bed rest is not needed for the treatment of acute lumbosacral strain.

90) Influenza virus vaccination reduces hospitalization and death from influenza and its complications in elderly and high-risk patients.

91) Always examine the feet and pedal pulses of diabetic patients regularly, looking for ulcerations, injury, or reduced blood flow.

92) Closely monitor patients with blood pressure measurements defined as "prehypertension, " and encourage lifestyle changes to prevent progression to hypertension.

93) Reduce the risk of hip fracture in elderly and high-risk patients with calcium and vitamin D supplements, exercise prescription, hip pads, and medications to treat osteoporosis, when indicated.

94) Assess a woman's risk of coronary disease, stroke, thromboembolism, and breast cancer before prescribing estrogen/progester one therapy in menopause.

95) Older adults currently constitute the fastest-growing population in the United States - a trend that is expected to continue for the foreseeable future.

96) Commonly used instruments for a comprehensive geriatric assessment include the Mini Mental State Exam, the Geriatric Depression Scale, activities of daily living, instrumental activities of daily living, and assessment of stability and mobility (e.g., Tinnetti or "Get Up and Go" test).

(7)

98) Delirium carries tremendous mortality and morbidity rates and should be identified, worked up aggressively, and treated as any medical emergency.

99) Diastolic dysfunction, as distinct from systolic dysfunction, 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. Although the

symptoms of diastolic and systolic dysfunction may be similar, the traditional therapy for systolic dysfunction can actually worsen ventricular filling and increase the risk of orthostasis and syncope in cases of diastolic dysfunction. 100) Fifteen percent of elderly patients who fall and fracture a hip report prior falls. It is essential to ask about falls, assess for fall risk, and then act accordingly, given the significant mortality and morbidity of hip fractures. Kaplan Videos – Neurology with Dr. Jacob

Kaplan Videos – Neurology with Dr. Jacob Levy, MDLevy, MD

Even if you do not know the answer to a question, try to think what the answer could be. Always ask what is the most likely diagnosis, why is it the most likely diagnosis, what is the next step in management (therapy vs. diagnostics), what is the first diagnostic test to order, what is the best or most accurate diagnostic test to order? Spinal Cord Compression

Spinal Cord Compression

* A 61yo AAM is brought to the ED complaining of back pain that started gradually three days ago. He describes the pain as band-like around the abdomen without radiation. His past medical history is significant for prostate cancer diagnosed three years ago. First thing to think about is if this is an emergency or not an emergency; meaning do we need to intervene right now or can we treat with something like analgesics and follow-up.

* The prostate cancer is important because metastatic disease to the spine could be compressing the spinal cord. Other worrisome cancers could be breast, lung, multiple myeloma, lymphoma. Other worrisome signs with back pain would be fever, urinary incontinence, urinary retention, fecal incontinence, sexual dysfunction in males, bilateral lower extremity weakness. So just the history of cancer with back pain means we should be evaluating this

acutely. If we’re suspecting spinal cord compression, we should see upper motor neuron lesion signs below the level of the compression. Signs would include hyperreflexia, increased tone, positive Babinski sign, spastic paralysis. * 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. If the compression is caught early enough when the patient is able to ambulate, their ability to ambulate after proper treatment is about 80%.

* Most likely diagnosis is spinal cord compression. Next step in the management of this patient is give

dexamethasone, not MRI of the spine, not x-ray, not bone scan. Consider therapy before diagnostics in management when the patient has an emergency. Best initial test is a spinal x-ray, sensitive maybe 80% of the time. Most

accurate test is MRI of the spine.

* Radiation therapy and surgical decompression are generally left for after the diagnosis is made. Say you gave dexamethasone and diagnosed, now there is an abscess or hematoma compressing the spinal cord, then do surgical decompression. Say it is lymphoma or cancer compressing the spinal cord, then do radiation.

Syringomyelia, Vitamin B12 Deficiency & Anterior

Syringomyelia, Vitamin B12 Deficiency & Anterior Spinal Artery InfarctionSpinal Artery Infarction

* A 25yo man comes to the Emergency Department status post motor vehicle accident. The ED physician has addressed the airway, breathing, circulation, and calls you to evaluate the patient. You perform a thorough neurological exam, finding (motor) lower extremity weakness 4/5 bilaterally with some hyperreflexia, (CN) cranial nerves intact, (sensory) pain/temperature lost on lower extremities, vibration/position intact, and light touch intact. * Most likely diagnosis is syringomyelia, with a pool of fluid developing in the spinal cord. Pain and temperature lost because these spinal cord tracts are centrally located (spinothalamic), while vibration/p osition and light touch are in posterior column.

* Best initial test for syringomyelia is an MRI. Most sensitive test is an MRI. Treatment is often surgical. If there is an anatomic problem in the spinal cord, there should be an anatomic solution.

* Vitamin B12 deficiency causes subacute combined degeneration of the cord. Characteristic signs of vitamin B12 deficiency are loss or proprioception and vibration with intact pain/temperature, usually with ataxia and pyramidal signs like hyperreflexia and positive Babinski.

* Anterior spinal artery feeds the sensory neurons involved in pain and temperature. So an anterior spinal artery infarct would have lost pain/temperature sense, sudden onset of flaccid paresis, and the presence of intact proprioception/ vibration sense.

* Patient presents with signs of cord compression. An MRI shows osteomyelitis compressing the anterior cord. Best test is MRI, first initial step is give dexamethasone. Best initial test is x-ray, even if they’re showing you M RI. Cerebrovascular Accidents (CVA)

Cerebrovascular Accidents (CVA)

* 56yo woman is brought to the ED by her daughter, complaining of sudden onset of right upper extremity weakness that started while she was watching television in the morning. Her daughter became concerned when her mother was

(8)

unable to talk in response to her questions. On neurologic exam, you note right upper extremity weakness with pronator drift and right facial palsy. When you question the patient, she seems to understand what is being said but

she cannot clearly respond.

* Most likely diagnosis is cerebrovascular accident (CVA). Pathophysiology is lack of blood supply to section of the brain. Could be an embolus coming from the atrium in a patient with atrial fibrillation. It could be a bleed in a

patient with hypertension. It could also be thrombosis, where the clot forms in the brain itself (not an embolus from a distant site). Hypotension can also induce ischemia, such as in a w atershed infarct.

* Focal neurologic deficit of sudden onset is very likely to be a stroke.

* Risk factors for cerebrovascular disease are the same as coronary artery disease, peripheral vascular disease, or carotid artery disease. General atherosclerosis risk factors include smoking, high cholesterol, diabetes, obesity, male gender, hypertension, increased age, HIV, and alcohol abuse.

* Important risk factors include atrial fibrillation, recent transient ischemic attack (TIA) with similar symptoms, valvular disease (especially mitral stenosis).

* There is an anterior circulation and a posterior circulation to the brain. Anterior is the middle cerebral artery (MCA) and anterior cerebral artery (ACA). Posterior is vertebral arteries forming the basilar artery and the posterior cerebral artery (PCA).

* Patients with MCA infarcts present with contralateral hemiparesis involving the face and the arm more extensively than the lower extremity. So, patient would have facial droop and weak upper extremity.

* Patients with ACA infarcts presents with contralateral hemiparesis involving the leg more than the face/arm. Mnemonic is “put your best foot forward” for foot/leg affected with forward/anterior artery. ACA ischemia may involve urinary incontinence and personality changes (Phineas Gage).

* Homunculus, “little man on your brain,” has to sleep comfortably at night. So he puts is feet up and lays back. Anterior circulation on interior (leg) and middle circulation on outside (arm/face).

* MCA infarct also comes with aphasia. Broca aphasia is expressive aphasia with intact understanding. Broca is broken speech. Wernicke aphasia is wordy, nonsensical speech, unable to understand. Aphasia occurs _{hemisphere stroke. Most people are left-hemisphere dominant.} with dominant

* Basilar artery provides blood supply to cerebellum, pons, and brainstem. Brainstem (medulla/pons/midbrain) is where cranial nerves are. So, patient could have sudden onset of diplopia, blurry vision, dysphagia, focal cranial nerve palsies. Cerebellar signs include ataxia and vertigo.

* With posterior circulation (basilar artery), deficit is contralateral if above decussation and ipsilateral if below. A cross syndrome is a cranial nerve deficit on one side, and a motor deficit (hemiparesis, ataxia) on the opposite side. Cross syndrome is most likely posterior circulation stroke.

* A cranial nerve III deficit (cannot adduct eye) on one side and hemiparesis on the other is Weber syndrome. * A cranial nerve III deficit on one side and ataxia on the other is Benedikt syndrome.

* A sensory loss on one side of the face with contralateral sensory loss on the body is Wallenberg syndrome. * PCA supplies occipital lobe, giving us the ability to see. PCA ischemia comes with hallucinations, visual loss. * 56yo woman is brought to the ED by her daughter, complaining of sudden onset of right upper extremity weakness that started while she was watching television in the morning. Her daughter became concerned when her mother was unable to talk in response to her questions. On neurologic exam, you note right upper extremity weakness with pronator drift and right facial palsy. When you question the patient, she seems to understand what is being said but

she cannot clearly respond.

* Patient has arm/face hemiparesis and Broca aphasia. Most likely diagnosis is M CA infarct (left side). Next step in management is head CT scan, not aspirin, not clopidogrel, not ticlopidine, not heparin, not transthoracic echo, not transesophageal echo, not tPA. Now, do we give contrast or no contrast? We are trying to distinguish between a bleed and ischemia, because these two have different management. Answer is head CT without contrast. We are

looking for the absence of blood. If there is no bleeding on the non-contrast CT, we assume ischemic stroke. * Most sensitive (accurate) test for diagnosing ischemic stroke is MRI. MRI most sensitive for posterior fossa lesions. CT scan without IV contrast is most sensitive test for hemorrhagic stroke.

* With ischemic stroke, look for reversible risk factors such as cardiac thrombosis (echocardiogram), carotid artery stenosis (carotid artery duplex, mainly for anterior circulation stroke), atrial fibrillation (24h Holter monitor). * Hemorrhagic stroke is managed by supportive care and consulting neurosurgery (poor prognosis). For ischemic stroke, we can think about giving aspirin, clopidogrel, heparin, tPA, ticlopidine.

* If patient has acute onset focal neurologic deficit, CT shows no bleeding, you are sure it is ischemic stroke, and symptom onset is within 3 hours, then answer is tPA/PLAT (tissue plasminogen activator).

(9)

* Must document time of onset and CT scan with diagnosis before giving tPA. If you give tPA past the 3-hour window, you’re only increasing their risk of bleeding. So the risk to benefit ratio is not favorable after 3 hours. * Contraindications for tPA therapy are bleeding (e.g. GI bleed, urinary tract bleed) within past 21 days, surgery within past 14 days, BP > 185/110, platelet count < 100,000, PT > 15sec, ischemic stroke or head trauma within 3 months, intracranial bleed ever in the past.

* Aspirin is used in ischemic stroke for secondary prevention. The benefit of aspirin in acute stroke is not as good as with acute myocardial infarction, but we give it anyway.

* Clopidogrel is used if the patient has failed aspirin therapy, meaning the patient is on aspirin after an ischemic stroke then has another ischemic stroke. Clopidogrel side effects include TTP and neutropenia.

* Ticlopidine is never the answer due to side effect, which are TTP and neutropenia. The difference between clopidogrel and ticlopidine is that ticlopidine causes the side effects (TTP, neutropenia) more often. * If the patient is allergic to aspirin, failed aspirin therapy, or is allergic to clopidogrel, add dipyridamole.

* Heparin reduces the rate of recurrent CVA. For every stroke you prevent, you cause one complication (e.g. bleed). So the only time you give heparin is when you have a higher risk of CVA. There is a higher risk of recurrent CVA if the patient has ischemic stroke with atrial fibrillation, basila r artery thrombosis, or stroke in evolution.

* Stoke in evolution is when symptoms are getting worse, a loss of brain function occurs with brain cell death. * Say you do a w orkup on the 56yo lady that has right-sided facial/arm hemiparesis. Carotid duplex finds 80% stenosis of the right internal carotid artery. Answer is not surgery. Indication for carotid endarterectomy (CEA) is >70% stenosis with symptoms. Symptoms mean you have to be able to blame a TIA or a stroke on the stenosis. If the patient’s symptoms were due to the carotid artery stenosis, the stenosis would be on the left side (not the right). * When looking at a CT scan to evaluate a suspected CVA, you’re looking for the presence of white material in the parenchyma of the brain. In ischemic stroke, the tissue will look darker than the surrounding tissue.

Seizures Seizures

* 29yo man is brought to the ED by ambulance after his mother found him convulsing in his bedroom. 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. The mother says he was tired and lethargic for 20 minutes after the episode. She then called the ambulance to bring her son to the hospital.

* What is the most likely diagnosis? Answer is seizure. Differentiate seizure from syncope, say due to arrhythmia. This patient was having convulsions (tonic-clonic movements). Patients who syncopize can have tonic/clonic movements. Urinary or bower incontinence is an important part of the history, but not necessarily specific. Bite marks on the tongue may imply seizure, but not specific either. The most specific thing on history for seizure is the post-ictal state. Patients who have syncope and come out will not be lethargic, tired, or with achy muscles. Syncope

has rapid recovery within minutes or seconds after unconsciousness. Here, the patient was tired/achy for 20minutes. So this is the clear differentiation.

* Urinary and bowel incontinence plus bite marks are seen more commonly in seizure than syncope. However, the post-ictal state still is the most specific symptom.

* A seizure is defined as random firing of neurons in the brain. A seizure is considered a complaint, like a patient coming in with chest pain; there is a large differential diagnosis for seizure.

* Ask yourself if there is an underlying cause for the seizure. Ask if the patient has a history of epilepsy. Do not assume that any seizing patient has a diagnosis of epilepsy.

* Seizure differential mnemonic: VITAMINS.

* Seizure: vascular (stroke, bleed, AVM), infection (encephalitis, meningitis), trauma, autoimmune (vasculitis, SLE), metabolic (electrolytes, glucose, drugs), idiopathic, neoplasti c (metastatic cancer, primary tumors), s for Psi or psychiatric (patient faking).

* If you’re thinking vascular disease, look for risk factors and sudden onset of neurologic focality. Suspect infection if the patient has seizure with fever, or nuchal rigidity, or photophobia. Suspect autoimmune if history involves a rash, purpura, low-grade fever with weight loss, arthritis, SLE stigmata, positive ANA. For metabolic, look at things like low sodium, high sodium, low calcium, low oxygen, low glucose, low magnesium. If a young woman with breast cancer has a seizure, think about metastatic to the brain.

* The next step in management is ABCs: airway, breathing, and circulation. Then benzodiazepine.

* 29yo man comes in with new-onset seizure witnessed by his mother, convulsing with a long post-ictal state, and the patient is already intubated. Blood pressure and circulation are intact. Patient is continuing to seize. What is the best initial treatment now? Answer is give lorazepam or diazepam, for acutely seizing patient.

* Always look for a secondary cause. If you identify a secondary cause, treat it, hoping seizures resolve. So if patient comes in seizing with sodium of 106, treatment would be focused on hypertonic saline. If patient came in

(10)

* If patient is continuing to seize without regaining consciousness between, this is status epilepticus. Management is lorazepam or diazepam.

* Say you give the benzo and the patient is still seizing. Then what do you give? Answer is phenytoin or fosphenytoin. Note, giving phenytoin IV is not recommended due to lack of solubility and resultant precipitation, give fosphenytoin instead.

* What if patient continues to seize after giving phenytoin or fosphenytoin? Give phenobarbital. * Next step after phenobarbital? Answer is midazolam and propofol (anesthesia).

* Seizure Meds: ABC, lorazepam/diazepam, phenytoin/fosphenytoin, phenobarbital, and last midazolam/propofol. * Seizures are categorized into partial, generalized, and complex vs. simple. Categories help determine what medication to give. A complex partial seizure is treated differently from a complex generalized seizure.

* A partial seizure only affects one part of the brain. So patient might have shaking/jerking of the hand, or the foot, or the leg. A generalized seizure affects the entire cortex. Either the seizure starts as generalized, or a partial seizure turns into a generalized seizure. A complex seizure implies loss of consciousness. A simple seizure has no loss of consciousness. An atonic seizure means lack of tone, so patient has “drop attacks.” An absence seizure is the opposite of an atonic seizure, so patient keeps postural tone but brain shuts down so the patient is not paying attention (no consciousness) and likely just blinking. Myoclonic seizures involve muscle jerks.

* What is the best test to identify abnormal neural activity that predisposes to a seizure? Answer is electroencephalogr am (EEG). So patient has first time seizure with no exact etiology, order an EEG.

* What if EEG is negative, when do you start treating an idiopathic seizure? Answer is w ith recurrent seizures. * So patient has normal neurologic exam, negative EEG, negative family history, and one seizure. We follow the patient. Once the patient has another seizure, we start treatment. If the patient has positive family history, we w ould

start right away at the first seizure.

* Medication for partial seizure (even one that becomes generalized) is carbamazepine or phenytoin. If carbamazepine or phenytoin are not answers, pick valproic acid.

* Medication for generalized seizure is valproic acid or lamotrigine. * Medication for absence seizure is ethosuximide.

* Medication for atonic or myoclonic seizure is valproic acid.

* Medication for unidentifiable seizure is valproic acid, as it is the most widely effective seizure medication. Parkinson Disease

Parkinson Disease

* A 56yo man is brought in by his wife for evaluation of a resting tremor that she noticed recently. She also states that her husband has been moving very slowly as of late. When questioned, the patient states that he feels fine and does not know why his wife is dragging him from doctor to doctor. His past medical history is significant for mild hypertension treated with a thiazide diuretic. Physical exam finds a resting tremor noted in his right hand, and when walking the patient is stooped forward m aking small steps. You note cogwheel rigidity in his right upper extremity with a positive Myerson sign (patient unable to resist blinking with glabellar tapping).

* Differential diagnosis for tremor includes Parkinson disease, essential tremor, and cerebellar disease. In Parkinson disease, the tremor occurs at rest and resolves with movement. In cerebellar disease, the tremor occurs primarily with movement (intention tremor). Exam for cerebellar disease would include finger-to-nose and heel-to-shin tests, with the patient have a compromised ability to reach the object. In Parkinson disease, the patient will have pill-rolling tremor at rest. In essential tremor, the tremor occurs and worsens with movement, there is a family history usually, and there are no other stigmata of cerebellar or Parkinson disease.

* So in the 56yo man with resting tremor, slow movement (bradykinesia, paucit y of movement), history of falls (postural instability), and cogwheel rigidity (arm feels like cogs on a wheel, moving in distinct steps), what is the most likely diagnosis? Answer is Parkinson disease. So, diagnosis of Parkinsonism is clinical.

* Normally when you walk and turn it is a smooth movement. With postural instability, patient turns in wide circle. * Causes of Parkinsonism are drugs (antipsychotics, metoclopramide, MPTP: an unintentional byproduct of the recreational drug MPPP), tumor, bleed or stroke, CO poisoning, cobalt, manganese. So ask yourself about secondary causes. Is this patient diabetic and taking metoclopramide for autonomic neuropathy with gastric paresis?

* Most cases of Parkinson disease are idiopathic, meaning we cannot identify a cause. * Parkinsonism is defined as death of dopaminergic cells in the substantia nigra.

* The drugs that cause Parkinson are antipsychotics, which are dopamine antagonists. You can decrease the amount of dopamine by antagonizing it (decreasing it directly) or by increasing acetylcholine. Acetylcholine acts to inhibit dopaminergic tone in the brain. So treatment is to either give dopamine to provide what is lost, or to take away acetylcholine so the dopamine in the brain can work more effectively.

* Dopamine agonists are bromocriptine, carbidopa/levodopa, pergolide, pramipexole, and ropinirole. Carbidopa inhibits the conversion of levodopa to dopamine in the periphery, so that the levodopa can reach the brain and be

(11)

converted to dopamine there; thus we can give less levodopa and get the same effect.

* Selegiline (MAO-B inhibitor), COMT inhibitors, and amantadine increase dopamine amount/effect also. * Acetylcholine blocking with trihexyphenidyl primarily.

* So how do you choose what to answer as the best initial treatment for Parkinson disease? First question to ask your self is what is the functional status of the patient? Meaning, how do they function on a day-by-day basis?

* Functional patients get amantadine or anticholinergic (e.g. trihexyphenidyl).

* Non-functional patients get carbidopa/levodopa, the most effective treatment for Parkinson disease. We don’t give carbidopa/levodopa to functional patients because it has the most serious side effects.

* Always ask how much function you are getting from the treatment at the expense of the side effects. * Side effects are psychosis, hypotension, and acute GI upset. After long-term therapy on carbidopa/levodopa, patients get response fluctuations. Response fluctuations are the “on/off phenomenon,” akinesia (restlessness), and

dyskinesia (abnormal movements). On/off phenomenon is quite distressing to patients.

* Say patient is functional and just has a tremor, pick amantadine if patient is > 65yo. Pick trihexyphenidyl if patient is < 60yo. We avoid anticholinergic medications in elderly patients because they can become confused, have urinary retention, dry mouth, dry eyes, more so than younger patients.

* Answer dopamine agonists (e.g. pramipexole, ropinirole) to treat response fluctuations for patients that are taking carbidopa/levodopa. You can also give a C OMT inhibitor or selegiline.

* If patient is on carbidopa/levodopa and it isn’t enough, add the dopamine agonist.

* The most preferred dopamine agonists are the newer ones, like ropinirole (not selegiline or COMT inhibitor). * Say patient has stigmata of Parkinson and you are asked what medication is thought to arrest the progression of Parkinson disease, the answer is selegiline.

Huntington Disease Huntington Disease

* 34yo man comes to your clinic for evaluation of strange spontaneous movements that have been occurring lately. Recently while sitting at a family dinner, the patient experienced uncontrolled grimacing with grunting. His family history is significant for his father who died at age 41 of dementia.

* Most likely diagnosis is Huntington disease. Know that patients will present with abnormal movement (chorea), abnormal behavior, loss of inhibition, changes in personality, and a family history of a similar thing happening to a first-degree relative (Huntington is autosomal dominant).

* Clinical diagnosis is presence of chorea with personality changes, usually in a patient 30-40yo with a positive family history. True diagnosis done with genetic analysis, looking for chromosome 4p CAG repeat.

* Treatment is supportive care; there is no formal treatment. Multiple Sclerosis (MS)

Multiple Sclerosis (MS)

* A 32yo woman comes to the ED with numbness and tingling in her right hand. She states that her symptoms began several days before admission and have progressively worsened over the last several hours. When asked, she states that three years ago she had an episode of seeing double that lasted two days that resolved on its own. Physical exam is significant for hyperreactive reflexes bilaterally in the lower extremities. You also note increased spasticity in her lower extremities.

* Most likely diagnosis is multiple sclerosis (MS).

* Differential includes MS, CVA, brain tumor, cervical spinal disease, and carpal tunnel syndrome. * CVA less likely because she is 32yo with no other listed risk factors.

* Brain tumor less likely as there is no specific tumor location giving lower extremity weakness along with diplopia. * Cervical spinal disease or carpal tunnel less likely because they do not explain the diplopia.

* The essential point for clinically suspecting MS is a patient with m ultiple neurologic deficits that are separated by space (anatomically) and by time (temporally).

* Testing includes MRI w ith gadolinium, CSF for oligoclonal banding, and olfactory/visual evoked potentials looking for abnormal transmission.

* What is the most sensitive/accurate test? Answer is MRI or brain and spine, 85-95% sensitive. Looking for multiple lesions and paraventricular lesions consistent with MS.

* The best initial test is also MRI, not CT scan, not lumbar puncture.

* If MRI is inconclusive or equivocal for the clinically suspected MS diagnosis, then get the lumbar puncture. * Olfactory/visual evoked potentials are not used much today with the development of MRI.

* Relapsing/remitting disease is a form of MS where patient goes through waxing/waning episodes of symptoms. * Relapsing/remitting disease can become progressive (secondary progression). Primary progressive disease has worsening MS symptoms right from presentation, least common, and worse prognosis.

* Treatment for acute exacerbation of M S is IV high-dose steroids with a 4-week taper on oral prednisone. Steroids do not slow down the progression of the disease, but they help symptomatically for the disease relapse.

(12)

* Medications useful to arrest the progression of MS are interferon beta 1a, interferon beta 1b, or glatiramer acetate. None of these three is better than the other. They have been shown to help with relapsing/remitting forms, but not in primary progression. No medication has been shown to help with primary progressive disease.

* Treatment for spasticity in MS is baclofen. * Treatment for fatigue in MS is amantadine.

* Treatment for urinary incontinence in MS is oxybutynin. * Treatment for urinary retention in MS is bethanecol. Dementia

Dementia

* A 67yo woman is brought to your clinic complaining of forgetfulness. She states that rec ently she has been forgetting telephone numbers and cannot remember the name of her mailman who she has known for 25 years. Her past medical history is significant for hypertension, coronary artery disease, and high cholesterol. Physical exam is

unremarkable.

* With memory loss, consider dementia and ask yourself if there is a reversible cause.

* Reversible causes: hypothyroidism (check TSH), vitamin B12 deficiency (check B12 level), frontal lobe neoplasm and chronic subdural hematoma (check for focality on exam or trauma history), syphilis (check RPR: rapid plasma reagin), uremia and cirrhosis (check creatinine, LFTs, physical exam), central or obstructive sleep apnea (look for obesity, speak with spouse), HIV.

* Non-reversible causes: Creutzfeldt-Jakob disease and prion disease (check for myoclonus, rapid dementia course usually weeks to months), Lewy body disease (delirium-like course, waxing/waning), multi-infarct dementia (stepwise progression, tie temporally dementia onset with CVA, difficult to differentiate from Alzheimer). * Most common cause of dementia is Alzheimer disease. In Alzheimer disease, there is initial memory loss that becomes chronic and gradual with relative preservation of social function and personality until late in the disease.

* Pick disease (frontal lobe degeneration) has personality changes initially, such as agitation, violence.

* Dementia is generally memory loss plus some other deficit in cognitive function, such as concentration, praxis, or executive function. This is where the mini-mental status exam (MMSE) is important.

* Patient presents with memory loss. Perform MMSE to find dementia. Then rule out or treat reversible causes. Then rule out non-reversible causes like Pick (personality changes first), CJD (myoclonus, rapid progression), multi-infarct dementia (temporal tie to CVA), and Lewy body (delirium-like). Now, we diagnose Alzheimer disease. * Treatment for Alzheimer disease was tacrine, but no longer used as the drug of choice due to liver toxicity. * Medication of choice for Alzheimer now is donepezil. Do not pick tacrine for first line.

Vertigo Vertigo

* A 53yo woman is brought to the ED complaining of dizziness. The patient describes walking to her bathroom and experiencing a sudden feeling of nausea. She managed to reach the bathroom where she vomited once and fell to the floor a second time. She was unable to get up off the floor and called 911. She describes the feeling of the room spinning around her even though she realizes she is not moving.

* Most important question is to identify what the patient means by dizziness. “Dizzy” is very nonspecific and does not have much significance medically. 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, light headed, palpitations, chest pain, shortness of breath. This implies cardiac disease.

* Vertigo is the sensation of movement in the absence of movement. Patient may say the room is spinning around me, the earth is rolling in front of my feet, like they are falling forward.

* Differentiating between vertigo and pre-syncope is a clinical determination.

* Next question after determining vertigo is if it is central (in the CN S, e.g. MS, posterior fossa tumor, medication) or peripheral (ear semicircular cannals). For central, we do M RI, for peripheral, we do symptomatic treatment. * Central vertigo is usually chronic, neighborhood signs (cranial nerve deficits via brainstem), pure nystagmus (in one direction, usually vertical), nystagmus non-suppressible with fixation, multi-directional nystagmus

* Peripheral vertigo is usually acute, hearing loss, tinnitus, mixed nystagmus (usually horizontal but with another component), nystagmus suppresses with fixation, uni-directional nystagmus

* Posterior fossa imaged more effectively with MRI than with CT scan.

* Ménière disease is a triad of (peripheral) vertigo, hearing loss, and tinnitus unrelated to head movement. Treatment of choice is diuretics, low salt diet, and surgical decompression if medical management fails. Disease is thought to be caused by swelling in the semicircular canals.

* Benign positional paroxysmal vertigo (BPPV) is peripheral vertigo of sudden onset related to movement of the head. Patient may say I move my head then 5-10 seconds later I get dizzy. Physical exam can reproduce symptoms via Dix-Hallpike test (head movement testing). Etiology is thought to be an otolith in the semicircular canals. Treatment of choice is movement exercises to try and move the otolith out of the canal.

(13)

* Labyrinthitis is peripheral vertigo that occurs when vertigo follows an upper respiratory tract infection. Treatment is meclizine (antihistamine) or diazepam in severe cases.

* So, if you find central vertigo signs on physical exam, do MRI imaging of the posterior fossa. If you identify peripheral vertigo, seek Meniere, BPPV, or labyrinthitis with their treatments listed.

* If you cannot identify a disease, give meclizine initially then diazepam secondary. Headache

Headache

* A 32yo woman comes into the office complaining of a headache that started two days ago. She locates her headache to the right side of her head and describes it as pulsating and throbbing in quality. The headache is worsened by walking up stairs or around the block. She admits to nausea but denies vomiting. She also states that loud noise and bright light exacerbate her pain. On exam, there is no focality on physical exam, she has had these headaches a few times before. M ost likely diagnosis is a migraine.

* Ask yourself, 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, fever, progressively worsening headache, symptoms aggravated by cough, worse in the early morning, aggravated by valsalva maneuver, nuchal rigidity, “worst headache of my life” (subarachnoid), thundercla p headache (time to peak pain was seconds), focality on CNS exam, headache occurs after vomiting, any headache starting at age > 55yo.

* Primary headache disorders include migraine, cluster, and tension.

* Migraines are associated with triggers, such as eating a specific food (e.g. chocolate), sleeping too little, stress, or during menstruation. A trigger is very specific for migraine.

* Pulsatile headaches occur in cluster and migraine headaches (both vascular).

* Photophobia and phonophobia (ligyrophobia) classically occurs in migraine but may occur in cluster also. * Cluster headaches are usually unilateral (like migraine), no trigger, has rhinorrhea, red eye, possibly Horner syndrome (ptosis, miosis, anhidrosis).

* Tension headaches are triggered by stress but not foods or emotion, are bilateral, vice-like, radiating to neck or back of the head.

* Migraines peak within 4-72 hours from onset of pain (gradual onset). Cluster headaches peak usually within 5 minutes (quick onset) and only last 45-90 minutes.

* Clusters happen 2-3 times per day over a 4-8 week period; occurring in clusters. * Management for tension headache is analgesics, like acetaminophen or NSAIDs.

* Management for cluster headaches starts with 100% oxygen. Next line is sumatriptan. Prophylaxis for cluster headaches includes lithium, prednisone, or verapamil.

* Management for mild migraine headache (no nausea or vomiting), give NSAIDs. If migraine is moderate to severe, abortive therapy is sumatriptan or ergot alkaloid. Prophylaxis for migraines is indicated when patient has more than 3 headaches per month. Prophylaxis is propranolol, timolol, or methysergide (generally not used because it causes retroperitoneal fibrosis).

* Never give sumatriptan to a patient with a history of coronary artery disease. Migraines are generally caused by vasodilation and sumatriptan constricts the vessels. So if a patient has a 70% left main coronary lesion and you give them sumatriptan, you just gave them an MI. Do not give it even if you have high suspicion of CAD.

Acute Inflammatory Demyelinating Polyradiculoneuropathy (AIDP) Acute Inflammatory Demyelinating Polyradiculoneuropathy (AIDP)

* A 46yo man is brought to your office complaining of rubbery legs. The patient states that his symptoms began two days ago. Approximately three weeks ago the patient states that he experienced several episodes of diarrhea that resolved spontaneously. On neurological exam, the patient is noted to have bilaterally lower extremity weakness with loss of reflexes.

* Most likely diagnosis is Guillain-Barré syndrome, an AIDP. CIDP (chronic) has a slower course, seen in HIV. * The distribution of weakness is important when differentiating between Guillain-Barré, myasthenia gravis (MG), and botulism. In Guillain-Barré, distribution starts in distal areas and moves proximal. Paresthesias (tingling) and autonomic instability (labile blood pressure, sweating) are also seen.

* Campylobacter jejuni infection (gastroenteritis) associated with Guillain-Barré syndrome (GBS). * Hyporeflexia seen in any peripheral neuropathy.

* The best initial test for the diagnosis of GBS is lumbar puncture, looking at CSF for high protein that is not accompanied by pleocytosis (a high number of cells). So you’re looking for high protein and few cells. * The best test (most accurate) for GBS is an electromyogram (EMG).

* Best initial treatment for GBS is intravenous immunoglobulin. You can also do plasmapheresis. IVIg and plasmapheresis are equivalent in their effect. Do not give prednisone or systemic steroids in the treatment of acute

(14)

Myasthenia Gravis (MG) Myasthenia Gravis (MG)

* A 35yo woman comes to the clinic complaining of double vision that seems worse near the end of the day. The patient also complains of difficulty chewing meat and other hard foods. She notices that her symptoms improve

following a good night sleep. On neurologic exam you notice snarling appearance when the patient is asked to smile and a nasal tone to her speech. You also note weakness of the upper extremities when the patient is asked to clench her fists around your fingers repeatedly.

* Most likely diagnosis is myasthenia gravis (MG).

* In MG, there typically is not a distal to proximal movement. Patients complain of easy fatigability, especially in the muscles of the throat and eyes (dysphagia, ptosis, diplopia). Symptoms are not acute either.

* MG is defined as muscle fatigue after repetitive motion of chronic onset with preferential involvement of the ocular and the pharyngeal muscles.

* The best initial test for diagnosing myasthenia is serology for the anti-acetylcholine receptor antibody. A tensilon test is not the initial test. In the context of clinical suspicion of myasthenia, anti-acetylcholine receptor antibody is extremely specific for the diagnosis.

* A positive tensilon test is not specific for the diagnosis; false positives seen in other diseases like amyotrophic lateral sclerosis (ALS, Lou Gehrig disease).

* Only answer tensilon testing when there is no answer choice for acetylcholine receptor antibody.

* 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 w eakness 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 – Pulmonology with Dr. Asher

Kaplan Videos – Pulmonology with Dr. Asher Kornbluth, MDKornbluth, 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 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-Capilla

Alveolar-Capilla ry ry Membrane DiffusionMembrane Diffusion