Ambulatory Internal Medicine

The 6 week Ambulatory portion of the 12 week Internal Medicine Clerkship is typically an outpatient, office based experience. The student has several options in various specialities to see what an internist does on a typical day. There is also the opportunity to spend some time in a hospital setting to see how the various "consulting" specialists function. As part of your experience, there are a series of lectures designed to cover some of the more basic topics that you learn about during your rotation. The following is a compilation of the answers to the discussion questions found in your Ambulatory packet put together by the clerkship directors.

Cardiovascular Disease
Management of Diabetes
Dyslipidemias
Management of Asthma and COPD
Basic Rheumatology and Joint Disease
Thyroid Disease and Osteoporosis
Management of Upper Respiratory Infection
Managment of Urogenital Problems

Cardiovascular Disease

Management of congestive heart failure

A. Definition: abnormality of cardiac function is responsible for the failure of the heart to pump blood at a rate commensurate with the requirements of the metabolizing tissues and/or to be able to do so only from an elevated filling pressure

• Class I: No symptoms

• Class II: Symptoms with ordinary activity

• Class III: Symptoms with less than ordinary activity

• Class IV: Symptoms at rest

B. Assessment: history, physical, CXR, ECG, CBC, electrolytes, creatinine, urea

Additional: echocardiography, nuclear studies, exercise electrocardiography

C. Treatment goals: reduce symtoms and decrease the need for repeat hospitalizations; 3, improve survival.

PRINCIPLES

I.Treat the underdlying cause of myocardial dysfunction

A.Increased demand: stress (physical, environmental, emotional), infection, fever, anemia, hyperthyroidism, HTN, pregnancy, valvular heart disease

B.Compliance/lifestyle: inadequate or improper medication intke, dietary indiscretion--salt and water excess, heavy alcohol consumption

C.Salt/water retention: medications (NSAIDs, steroids, TCAs, chlorpropamide), renal disease

D.Decreased pump fcn: negative inotropic medications (beta-blockers, CCBs, anti-arrythmics, chemotherapeutic agents), arrhythmias, ischemia/infarction, pulmonar embolism, radiation Tx

II.Adequate management of risk factors

A.Hypertension

B.Diabetes

C.Hyperlipidemia

D.Cigarette smoking

III.Salt restriction

IV.Education and counselling: disease understanding, early recognition of s/s, compliance with medications, light activity

V.Medications

A.Diuretics

1. Major therapeutic management--Second line

2. Reduce excessive salt and water retention, reduce preload, decreases symptoms from pulmonary and systemic congestion.

3. Rarely to be used as a single agent

4. Loop diuretic

5. Caution with serum electolytes, urea and creatinine

B.Digitalis and other inotropic drugs--Third line

1. Phosphodiesterase inbibitors are not recommended

2. Dobutamine not recommended except in select patients with intractable heart failure

3. Digoxin for A-fib plus CHF

4. Digoxin for pts with sinus rhythm for relief of symptoms and exercise tolerance

5. Repeat measures of digoxin levels if poor compliance suspected

C.Vasodilators

1. ACEI therapy has been shown to reduce mortality, improve quality of life, and reduce the risk of myocardial infarction--First line DOC

2. Patients with the lowest ejection fraction and worst symptoms derive the most benefit from ACEI therapy.

3. ACEI strongly recommended in symptomatic patients to improve survival.

4. ACEI strongly recommended in asymptomatic patients with moderate left ventricular dysfunction (LVEF 35% or less)

5. ACEI strongly recommended in patients with renal infarction and moderate left ventricular dysfunction (LVEF 40% or less)

6. Nitrates with hydralazine are recommended to improve exercise tolerance

7. CCBs are not recommended for routine use

8. Others (prazosin, minoxidil, alpha-methyl-dopa) are not recommended

D.Beta-blockers

1. Not recommended as routine therapy

2. Recommended in symptomatic patients with an underlying congestive cardiomyopathy for relief of symptoms and decreased need for cardiac transplantation

E.Antiarrhythmic drugs, pacemakers, devices

1. Antiarrhythmic therapy for asymptomatic arrhythmias is not recommended

2. Type I antiarrhythmic drugs should be avoided (quinidine, procainamide, disopyramide, flecainide, propafenone)

3. Sotalol and amiodarone are recommended for symptomatic arrhythmias

4. Rapid heart rates with A-fib require verapamil, beta-blocker or sotalol

F.Anticoagulants

1. Anticoagulant therapy is strongly recommended in all patients with heart failure and associated A-fib

2. Use warfarin therapy unless at risk then use ASA

3. Anticoagulation is not recommended as a routine in patients with sinus rhythm

VI.Emergent care

A. Assessment: underlying etiology, precipitating or aggravating factors

B. General: positioning (trunk up, legs down) and oxygen Tx. Furosemide and morphine initially depending on volume status

C. Intensive: parenteral vasodilators and positive inotropes

Management of atrial fibrillation

I. The most common sustained arrhythmia encountered in clinical practice. A major cause of stroke. Palpations most common but may include: fatigue, dyspnea, dizziness.

II. Three therapeutic goals: rate control, maintenance of sinus rhythm, prevention of thromboembolism

A.Rate control

1. With ventricular preexcitation, acute rate control best with: IV verapamil, diltiazem, or -adrenergic blockers (especially for thyrotoxicosis and increased sympathetic tone).

2. Digoxin should be considered first-line theapy with CHF

B.Maintenance of sinus rhythm

1. No drug proven superior to another: quinidine, procainamide, disopyramide, propafenone, sotalol, flecainide, and amiodarone.

2. IV procainamide is the doc for WPW

C.Prevention of thromboembolism

1. Low risk patients: 325 mg/day ASA

2. High risk patients: warfarin

a. Three weeks of anticoagulation before cardioversion for A-fib of unknown duration or >48 hours, and continued for four weeks after. Alternative is heparin and TEE to asses thrombus formation

Management of angina pectoris

I. Coronary artery disease continues to be the leading cause of death and diability in the United States.

II. Imbalance between myocardial oxygen demand and coronary blood flow: reduction in coronary blood supply or by increase in myocardial oxygen demand

III. Three areas: modification of risk factors, evaluation, medical management

A.Modification of risk factors:

1. Significant long-term reduction in death rate in patients with CAD and transient episodes of myocardial ischemia

2.Cigarette smoking

3.Systemic hypertension

4.Elevated serum cholesterol levels

B.Evaluation

1.Known risk factors: DM, HTN, smoking, poor lipid profile, FHx, abnormal ECG or CXR

2.Exercise ECG

a. induces ischemia in a controlled setting

b. atypical symptoms, pts with a chronic stable angina or those with a pevious MI

c. 68/77

3.Exercise Thallium

a. Myoardial uptake of Tl201 is proportional to regional myocardial blood flow and dependent on the presence of viable myocytes

b. Technetium and Teboroxime

c. Expensive, radiation exposure

d. 84/87

4.Dipyridamole

a. Unable to do exercise tests. Like adenosine, coronary artery vasodilator which augments flow in normal coronary arteries as much as 5x, flow in diseased arteries does not change appreciably; gives a flow differential.

b. CI in patients with severe reactive airways disease and may provoke bronchospasm

c. 86/71

5.Adenosine

a. Advantages over dipyridamole include its direct action, shorter half-life and vasodilatory effect.

b. More side effects; CI with RAD and AV block

c. 88/85

6.Dobutamine

a. Increase th heart rate, blood pressure, and contractility and therby induce true ischemia

b. Frequent side effects

c. Safe with asthma

d. 80-97/80-97

7.Positron emission tomography

a. Cost-effective in replacing need for angiograms

b. 96/96

8.Echocardiography

a. Detect ischemia-induced regional wall-motion abnormalities that occur during stress testing

b. With exercise 88/80

c. With dobutamine 86-96/66-95

9.Radionuclide ventriculography

a. Tc99m-labeled erythrocytes to assess ventricular function and regional wall motion

b. 85-90/90

Clincal presentation	Test
Typical angina, normal ECG	Exercise ECG
Typical angina, women with positive exercise treadmill test (ETT), equivoval ETT, abnormal baseline ECG	Exercise with thallous chloride Tl-201 or technetium Tc99m sestamibi imaging
Typical angina, unable to exercise	Dipyridamole or adenosine scintigraphy
Atypical chest pain High exercise capacity Low exercise capacity or blunted HR response on antianginal therapy	exercise, with or without scintigraphy Adenosine or dipyridamole
Poor exercise tolerance, moderate to severe bronchospastic airway disease, or both	dobutramine echocardiography with or without scintigraphy
large body habitus	stress with Tc99m sestamibi imaging
potentially unstable ischemic disease (recent ischemia or severe heart failure)	adenosine scintigraphy
left bundle branch block, paced rhythm, frequent ectopy	adenosine or dipyridamole scintigraphy

C.Medical management (anti-ischemic trug therapy)

1.Nitrates

a. Preferred agents to alleviate an established attack of angina regardles of the underlying mechanism

b. M: peripheral venodilation (dec. preload), arterial vasodilation (dec. afterload) at higher doses, and vasodilation of coronary vessels

c. Overall, decrease ventricular wall stress

d. Tolerance develops with long-term contiuous use

2.Beta-adrenergic blockers

a. Bind specific receptors in cardiac muscle, inhibit the binding of catecholamines with resultant attenuated cardiac response seondary to sympathetic stimulation

b. Reduction in heart rate at reat, attenuation of the degree of heart rate response to exertion, decrease in blood prssure, decrease in the force of contraction

c. Especially useful in exertional angina

d. SE: caution with bradyarrhythmias or AV conduction abnormalities, or with CHF; reactive airway dz, peripheral arterial insufficiency, and DM

e. When tolerated, the most effective antianginal drugs for most patients with stable CAD.

3.Calcium Channel Antagonists

a. Relative restriction of calcium influx into the cell leading to a variety of hemodynamic and electrophysiologic effects.

b. Significant vasodilation at the level of coronary and systemic arterial beds, decrease myocardial contractility, and depress the automaticity and conduction of the SA and AV nodes.

c. Increase coronary blood flow and decrease myocardial oxygen demand by afterload reduction and a decrease in myocardial contractility

d. Safe with RAD, peripheral arterial insufficiency and DM

5. Treat with ACEI whether hypertensive or not.

Dyslipidemia

Be able to apply the NCEP II guidelines to patient management.

Risk factors: age, male, family history, CHD, smoking, HTN, diabetes, cholesterol

Serum cholesterol needs to be measured every 5 years in people over 20 years old (non-fasting)

I.Initial classification is based on total cholesterol and HDL cholesterol

A.Less than 200 total

1.HDL <35 mg/dL proceed to lipoprotein analysis (LA)

B.Total cholesterol 200-239

1.HDL >35 and < 2 risk factors get lifestyle management; repeat in 2 years

2.HDL <35 or 2+ risk factors get LA

C.Total cholesterol >240 get LA

II.Lipoprotein Analysis is the next step; ten hours fasting

A.Desirable LDL cholesterol (<130) gets education only; repeat in five years

B.Borderline LDL (130-159)

1.<2 risk factors gets lifestyle management

2.2+ risk factors gets clinical evaluation and diet therapy

C.High risk LDL (>160) gets clinical evaluation and diet therapy

III.Coronary heart disease has different standards

A.LA must have LDL cholesterol <100 mg/dL

IV.Treatment based on LDL level

Patient category	Initiation level	LDL goal
Dietary therapy
Without CHD and <2 RF	>160	<160
Without CHD and 2+ RF	>130	<130
With CHD	>100	<100
Drug Treatment
Without CHD and <2 RF	>190	<160
Without CHD and 2+ RF	>160	<130
With CHD	>130	<1--

Identify the major classes of lipid-lowering agents and the effects of each on LDL, HDL, and triglycerides.

1. Cholestyramine and colestipol: Bile-acid binding resins; lower concentrations of LDL cholesterol

2. Niacin: Mechanism not known; decreases tricglycerides, total serum cholesterol and cholesterol, and increases HDL cholesterol; also lowers lipoprotein (a); lower mortality rate

3. HMG-CoA reductase inhibitors: inhibit the enzyme that catalyzes the rate-limiting step in cholesterol synthesis; most effective drug in lowering plasma concentrations of low-density-lipoprotein (LDL) and total cholesterol.

4. Gemfibrozil: Fibric acid derivative that decreases synthesis of apolipoprotein B, lowers VLDL and can increase HDL cholesterol; lowers plasma triglycerides; does not decrease mortality.

5. Fish oil: Long-chain, highly unsaturated omega-3 fatty acids; decrease triglycerides and cause small decreases in LDL cholesterol, without affecting HDL cholesterol.; decreased mortality shown.

Identify the most common side effects for the following:

Niacin: Flushing, pruritis, GI distress (take with aspirin to prophylax); blured vision, glucose intolerance, hyperuricemia, dry eyes or hyperpigmentation; hepati toxicity

Cholestyramine: Constipation, heartburn, nausea, belching, and bloating; Fat malabsorption

Gemfibrozil: Upper gastrointestinal symptoms, potentiate effect of oral anticoagulants, increase biliary cholesterol saturation increasing formation of cholesterol gallstones

HMG Co-A reductase inhibitor: Mild, transient GI disturbances, rash, and headache, sleep disturbances, inc. plasma aminotransferase activities, lupus-like syndrome, severe myalgia

Define primary vs. secondary prevention with regards to the treatement of hyperlipidemias.

Primary prevention: Clinical management of patients without CHD

Secondary prevention: Treatment of elevated LDL cholesterol in patients with prior CHD and/or other atherosclerotic disease

Be able to calculate the LDL cholesterol given the total cholesterol, HDL and tryglyceride.

LDL cholesterol = (Total cholesterol - HDL cholesterol) - (Triglycerides/5)

High risk LDL: >160 gm/dL

Borderline-high-risk: 130-159 mg/dL

Desirable LDL cholesterol < 130 mg/dL

Be aware of the cost of the various lipid-lowering agents.

Amounts shown for a daily dose.

Understand the indications for and the interpretations of peak flow monitoring and pulmonary function tests.

Asthmatics often have a poor recognition of symptoms and poor perception of severity of disease, thus it is important to have some objective measures of airflow obstruction and variability. PFMs and PFTs provide a way to objectively assess pattern and severity of airflow obstruction. This type of testing is indicated in all persons affected with airwary difficulties.

Spirometry is a tool used to measure forced expiration, air flow and volume. The pattern of flow that result from a forced expiration test can reveal obstructive (decreased flow) or restrictive (decreased volume) diseases by the shape of the curve

Further testing to obtain additional information include: DLCO, lung volume measurements with radioactive materials, bronchial provocation with irritating substances, cardiopulmonary exercise tests with similar ventilatory measures to assess various lung volumes.

5 factors implicated in acute deterioration of asthma / COPD

1. Patient is high risk for asthma exacerbations

2. Exacerbation is severe

3. Response to bronchodilator is not prompt

4. Beta2-agonist needed every 3-4 hours instead of 24-48 hours

5. No improvement within 2-6 hours of starting corticosteroid therapy

6. Clinical features: cough, breathlessness, wheeze, chest tightness, accessory muscles, retractions

Identify mechanisms of action and common side effects of therapies for asthma / COPD

Inhalation is better than systemic or oral treatment, spacers decrease systemic side effects

I.Brochodilators

A.Beta2-agonist

1.M: relax smooth muscle, enhance mucociliary clearance, decrease vascular permeability, modulate mediator release from mast cells, last 4-6 hours, short-acting agonists are the DOC

2.SE: cardiovascular stimulation, skeletal muscle tremor, hypokalemia, hyperglycemia

B.Methylxanthines

1.M: Mechanism unlcear, stimulate respiratory drive, reduce inflammation, increase mucociliary clearance, increase collateral circulation

2.SE: GE, variable metabolism depending on individual, arrythmias and CNS problems

C.Anti-cholinergics

1.M: block postganglionic efferent vagal pathways, less potent, longer time for onset, use as an alternative

2.SE: excessive sympathetic (no counteractive parasympathetic)

II.Anti-inflammatories

A.Sodium cromylate

1.M: mechanism unknown, inhibits IgE mediated release of antihistamines, suppresses other inflammatory cells

2.SE: minimal, coughing

B.Nedocromil sodium

1.M: 4-10x more potent, reduces non-atopic asthma, improves lung function

2.SE: none

C.Corticosteroids

1.M: most effective, interfere with arachodonic acid metabolism, synthesis of leukotrienes and prostaglandins, inhibit cytokines, decrease immune response

2.SE: adrenal failure, fatal varicella, wash mouth to avoid candida

III.Other medications

A.Ketotifen (H₁-antagonists)--inconsistent evidence that it helps

B.Gold, methotrexate, btroleandromycin et al immunosuppressants still experimental

C.Acupuncture, homeopathy, ionizers and other complimentary treatment not proven

Stepped therapy approach to Asthma / COPD

Rheumatology / Joint Pain

Describe the historical and physical exam features of fibromyalgia syndrome.

Historical: diffuse achiness (more axial), stiffness (worse in the morning), and fatigue. Symptoms commonly exacerbated by environmental stimuli. Other problems include: IBS, tension HAs, paresthesias, sensation of swollen hands.

Physical exam: multiple tender points in specific areas. May have no underlying disease or may have concomitant entities as diverse as RA, OA, Lyme dz, or sleep apnea. Strong female predominance (>75%), peak incidence in 20-60 year-old age group

Diagnosis: widespread pain in combination with tenderness of at least 11 of 18 specific tender point sites, disabling fatigue of at least 6 months duration.

Differential: myofascial pain, polymyaliga rheumatrica, axial arthritis, hypothyroidism, electrolyte imbalance, osteomalacia, metabolic myopathies, eosinophilia-myalgia syndrome, early collagen disease, psychogenic rheumatism, and chronic fatigue syndrome. Infectious: EBV, Lyme spirochete, HIV, parvovirus B19.

Outline a treatment strategy for fibromyalgia.

1. Patient education and reassurance.

2. Medical: Amitriptyline, cyclobenzaprine, alprazolam. NSAIDs and corticosteroids have not been effective as single agents.

3. Non-pharmacologic: psychological counseling, acupuncture, occasional tender point injections (local anesthetics or corticosteroids), ultrasound treatments, massage, and exercise (aerobic).

Compare and contrast the pathophysiology, physical exam findings, natural history, and treatment of rheumatoid arthritis and osteoarthritis.

I.Pathophysiology

A.RA: Initial event appears to be activation and/or injury of synovial microvascular endothelial cells. Increased plasma exudation. Progression involves hypertrophy of synovium with edema and innumerable villous projections of synovial tissue protrude into the joint cavity. Characteristic events include: neutrophil accumulation in synovial fluids, macrophage accumulation in rheumatoid synovium, T lymphocyte cytokines in larger amounts, angiogenesis, chondrocyte and extracellular cartilage matrix loss, neuropeptide release.

B.OA: Loss of articular cartilage represents the pathologic hallmark of OA; remodeling and hypertrophy of bone are also major features (osteophytes). Not a disease of the cartilage, rather a failure of an organ--the diarthrodial joint. Develops in two settings: when the biomaterial properties of the articular cartilage and underlying subchondral and bone are normal, but excessive loads on the joint cause the tissues to fail; or when the applied load is reasonable but the biomaterial properties of the cartilage or bone are inferior.

II.Physical exam findings

A.RA: joint immobilization, muscle spasm and shortening, bone and cartilage destruction, ligamentous laxity, altered tendon function.

1. Joint manifestation: C-spine (rare), shoulders (more common than hip), elbow (easiest to detect inflammation, hand (virtually all pts in wrist, MCP, and PIP while DIP are spared; swan neck deformities, tenosynovitis in extensor pollicus longus), hip (late), knee (easily detected), foot and ankle (infrequent);

2. Skin manifestations: rheumatoid nodule (extensor surfaces, pressue points), vasculitic lesions;

3. Ocular manifestations: scleritis, ketatoconjunctivitis sicca;

4. Respiratory manifestations: inflammation of the cricoarytenoid joint giving laryngeal pain, dysphonia and pain on swallowing; interstitial lung disease;

5. Cardiac: inflammatory pericarditis

6. Gastrointestinal: none, but PUD and gastritis with NSAID Tx

7. Renal: secondary to Ts

8. Neurologic: myelopathies d/t C-spine instability, entrapment neuropathies, ischemic neuropathies (mononeuritis multiplex);

9. Hematologic: hychromic-microcytic anemia with low iron and low IBC is almost universal, Felty's syndrome (RA, splenomegaly, leucopenia--neutrophilic, lymphadenopathy, thrombocytopenia, HLA-DR4 haplotype)

B.OA: Most common joint disease. Pain in the involved joint, which is typically worse with activity and relieved by rest; stiffness after periods of immobility (gelling); enlargement of the joint; instability; limitation of motion;and functional impairment. Crepitus. Periarticular muscle atrophyis common and the associated weaknes may contribute to disability.

1.Hand: Heberden's nodes are spurs at dorsolateral and medial aspects of the DIP joints, similar nodes at PIP joints are called Bouchard's nodes.

2.Knee: localized tenderness over various components of the joint and pain on passive or active motion, crepitus, muscle atrophy, chondromalacia patellae in young adults with softening and erosion of patellar articular cartilage;

3.Hip: limp, pain localized to the groin or along the inner thigh, loss of hip motion (most marked on internal rotation or extension);

4.Foot: first MP joint

5.Spine: cauda equina syndrome, spinal stenosis

III.Natural history

A.RA: uncertain, variable. Factors that predict a more sever course include the presence of RF, nodules, and the HLA-DR4 haplotype. If a joint is to become involved, it will do so 90% of the time in the first year. 10-15 years less life in patients with severe form (d/t infections, pulmonary and renal dz, GI bleed)

B.OA: Pain early in the disease occurs after joint use and is relieved by rest. Later, pain occurs with minimal motion or even at rest. At this stage of the disease, night pain is common.

IV.Treatment

A.RA: Patient education, balance between rest and exercise and medication (Aspirin, NSAIDs, corticosteroids, SAARDs)

1.SAARDs: auranofin, azathioprine, chlorambucil, cyclophosphamide, cyclosporin, parenteral gold salts, hydroxychloroquine, methotrexate, penicillamine, sulfasalazine

B.OA: Physical therapy, weight reduction, protection of joints, drug therapy (acetominophen, newer NSAIDs), surgery, experimental agents

Describe the mechanism of action for NSAIDs

1. Suppression of proinflammatory and pain-enhancing prostaglandin synthesis at sites of inflammation

2. Positioning of NSAID molecules within the cell membrane and consequent modulation of neutrophil intracellular signaling, leading to decreased neutrophil migration to inflammtory sites and down-regulation of the releas of fre-radicals and destructive enzymes at these sites

List the side effects of the NSAIDs.

I.Gastrointestinal

A.Dyspepsia, nausea, vomiting, diarrhea, constipation

B.Esophagitis, esophageal ulcer

C.Gastric and duodenal mucosal erosions, ulcers, bleeding perforations

D.Small-and large-bowel ulcers, diaphragm-like strictures (uncommon)

II.Renal

A.Hemodynamic renal failure (ranging from inc. creat. clearance to ARF)

B.Interference with salt/water excretion (HTN, CHF, pedal edema)

C.Hyperkalemia

D.Interstitial nephritis (uncommon)

III.Hematologic

A.Increased bleeding time (dec. platelet aggregation)

B.Bone marrow depression (rare)

IV.Central nervous system

A.Sedation, confusion, HA

B.Depression, psychosis (espec. indomethacin, but rare)

C.Tinnitus (espec. salicylates)

D.Coma (salicylate intoxication)

V.Hepatic

A.Increased transaminase levels (common)

B.Clinical hepatitis (uncommon)

C.Hepatic failure (rare)

VI.Pumonary

A.Worsening chronic obstructive pulmonary disease

B.Asthma

VII.Other

A.Rash

B.Photosensitivity

Understand when to order lab tests appropriately for RA and SLE.

1.RA: No laboratory test, histologic, or a radiographic finding that conclusively indcates a defininitive diagnosis of RA. Rheumatoid factor (in serum of about 85% of RA pts, correltates with severe disease), ESR (quantifies level of inflammation at the time of the test), C-reactive protein (acute phase reactant)

2.SLE: cytopenias including anemia, leukopenia (even with active disease), lymphopenia, and thrombocytopenia are frequent manifestations of SLE

Osteoporosis and Thyroid Disease

Interpret the results for common thyroid laboratory tests

I.TSH low

A.T4 low--pituitary

B.T4 high--hyperparathyroid, exogenous thyroid, Graves, hot nodule

II.TSH high

A.T4 low--hyperpituitary, central brain tumor

B.T4 low--primary hypothyroid

Describe the evaluation of the patient with a solitary thyroid nodule.

I.History: over 60, smoker, voice change, history of radiation exposure, hypo- / hyperthyroid symptoms

II.PE: hypo- / hyperthyroid (usually normal with CA), nodules, node enlargement

III.Tests: fine needle aspirate, thyroid scan

IV.Tx: surgery for malignancy, medical therapy for benign nodules (L-thyroxine)

V.High risk for malignant neoplasm

A. medullary thyroid cancer (MEN in family), rapid tumor growth, very firm nodule, fixation to adjacent structures, vocal cord paralysis, enlarge regional lymph nodes, distant metastases

VI.Moderate suspicion for malignant neoplasm

A. Age <20, age >60, history of neck irradiation, male sex and solitary nodule, dubious fixation, diameter >4 cm and partially cystic

VII.Low suspicion of malignant neoplasm

A. All others

Identify the risk factors for the development of osteroporosis

White or asian, smoking, caffeine, thin habitus, sedentary, family history, excessive alcohol, prolonged calcium deficit, nulliparity, estrogen deficient states and long-term medications (steroids, phenytoin, thyroxine)

Describe the treatment options for osteoporosis

I.Prevention

A.Calcium, good general nutrition, regular exercise, discourage smoking, vitamin D

B.Optimize bone mass

C.Preserve skeletal integrity

II.Treatment goals

A.Prevent fractures

B.Stabilize bone mass

C.Relieve symptoms of fracture / deformity

D.Maximize physical function

III.Treatment

A.Calcium and Vitamin D supplementation--1500 mg/day with meal

1.EFF: reduces rate of bone loss

2.SE: constipation

3.CI: hypercalciuria

B.Estrogen--625mg/day,standard of care

1.EFF: 50% reduction in fractures, decrease CV problems

2.SE: endometrial hyperplasia (add progestin to eliminate), irregular bleed, cholelithiasis, risk of increased breast CA controversial

3.CI: undiagnosed bleed, pregnancy, CA, thromboembolic history, liver problems

C.Bisphosphates--10mg/day, good alternative to estrogen

1.EFF: increase BMD in vertebrae, femoral neck, femoral trochanter (8%, 6%, 7%)

2.SE: mild GE, strictures, esophagitis

3.CI: hypersensitivity

D.Calcitonin--alternative to estrogen / alendronates (200 ug/day)

1.EFF: increased body calcium for one year, little BMD increases; nasal spray did increase lumbar BMD

2.SE: N/V, inflammatory reaction, flushing, GI problems

3.CI: hypersensitivity

4.Better for acute fx, add-on

Describe the indications, risks, and benefits of hormone replacement in the postmenopausal woman.

I.Indications

A.Low estrogen states

1.Post-menopausal

2.Hysterectomy / bilateral oophorectomy

II.Risks

A.Increased risk of breast cancer after long duration (>15 years) of estrogen replacement~controversial.

B.Endometrial cancer (controlled by progestin use)

III.Benefits

A.Fewer fatal coronary heart disease events.

B.Fewer deaths from hip fractures.

C.Significant reduction of all-cause mortalitiy

IV. The use of progestins in combination with estrogens is generally advised in the US for women who have not undergone hysterectomy.

V. When a sufficient dose and duration of progestins are used, therapy appeares to be highly effective in reducing the risk of endometrial cancer associated with estrogen use.

Upper Respiratory Infections and Allergies

5. Bronchoscopy

Urogenital Disease

Identify the three major causes of vaginitis and list important physical and laboratory exam findings which help in their differentiation.

1. Candida: patchy colonies adherent to vaginal wall, thick cheesy discharge, KOH prep

2. Trichomonas: abundant discharge; wet mount shows motile trichomonads.

3. Bacterial vaginosis: scant, fish-odored discharge; wet mount reveals clue cells with absent lactobacilli; pH >4.5

Outline a treatment strategy for the various causes of vaginitis.

1. Candida: miconazole 3-7 days

2. Trichomonas: metronidazole

3. BV: metronidazole

List important causes of dysuria in women.

1. Vaginitis (candida or trichomonas)

2. Cystitis

3. Pyelonephritis

4. Urethritis (Chlamydia trachomatis, Neisseria gonorrhoeae, or HSV)

Identify the most common organisms isolated in women with urinary tract infections.

1. E.coli~80%

2. Staph saprophyticus~5-15%

3. Klebsiella species

4. Proteus mirabilis

List 4 common antibiotic classes used to treat urinary tract infections.

1. Trimethoprim-sulfamethoxazole

2. Cephalosporins

3. Fluoroquinoloines

4. Penicillinase-resistant penicillins

List common symptoms of benign prostatic hyperplasia.

1. Frequency of urination

2. Nocturia

3. Urgency

4. Straining to urinate

5. Hesitancy

6. Weakness of urine stream

7. Intermittent stream

8. Sensation of incomplete emptying

Identify the medical therapies for BPH and their mechanisms of action.

1. Watchful waiting. Periodic reassessment of symptom level, physical findings, routine laboratory testing and optional urologic diagnostic procedures.

2. Surgery. Best chance for symptom improvement. Highest rate of significant complications. Transurethral resection most common followed by transurethral incision.

3. Balloon Dilation. Fewer complications and less effective than surgery. Temporary with frequent recurrence.

4. Alpha Blockers. Alpha₁-adrenergic receptor blockers such as doxasozin (Cardura), prazosin (Minipress) and terazosin (Hytrin), relax smooth muscle of the bladder neck and prostate. Non-selective alpha blockers have too many side effects.

5. Finasteride (Proscar). 5-alpha reductase inhibitor blocking conversion of testosterone to dihydrotestosterone, the major intraprostatic androgen in men. Reduces the size of the prostate.

Describe the diagnosis and treatment of common sexually transmitted diseases.

1. Chlalmydia: genital swab specimens; doxycycline or azithromycin

2 Gonorrhea: genital swab specimen; ceftriaxone

3. Epididymitis: chlamydia and gonorrhpeae usually; ofloxacin if pathgen not known.

4. PID: Chlamydia or gonorrhoeae et al; cetriaxone and doxycycline

5. Trichomoniasis: wet prep; metronidazole

6. Bacterial vaginosis: wet prep and KOH; metronidazole

7. Vulvovaginal candidiasis: pelvic; miconazole suppositories

8. Syphilis: VDRL, FTA-ABS; penicillin G

9. Chancroid: culture; ceftriaxone

10.Pediculosis and Scabies: microscope exam; permethrin 5%

11. Genital warts: observtion; podophyllin or cryotherapy

12. Genital herpes: Tzanck test; acyclovir

Urogenital Disease

Identify the three major causes of vaginitis and list important physical and laboratory exam findings which help in their differentiation.

1. Candida: patchy colonies adherent to vaginal wall, thick cheesy discharge, KOH prep

2. Trichomonas: abundant discharge; wet mount shows motile trichomonads.

3. Bacterial vaginosis: scant, fish-odored discharge; wet mount reveals clue cells with absent lactobacilli; pH >4.5

Outline a treatment strategy for the various causes of vaginitis.

1. Candida: miconazole 3-7 days

2. Trichomonas: metronidazole

3. BV: metronidazole

List important causes of dysuria in women.

1. Vaginitis (candida or trichomonas)

2. Cystitis

3. Pyelonephritis

4. Urethritis (Chlamydia trachomatis, Neisseria gonorrhoeae, or HSV)

Identify the most common organisms isolated in women with urinary tract infections.

1. E.coli~80%

2. Staph saprophyticus~5-15%

3. Klebsiella species

4. Proteus mirabilis

List 4 common antibiotic classes used to treat urinary tract infections.

1. Trimethoprim-sulfamethoxazole

2. Cephalosporins

3. Fluoroquinoloines

4. Penicillinase-resistant penicillins

List common symptoms of benign prostatic hyperplasia.

1. Frequency of urination

2. Nocturia

3. Urgency

4. Straining to urinate

5. Hesitancy

6. Weakness of urine stream

7. Intermittent stream

8. Sensation of incomplete emptying

Identify the medical therapies for BPH and their mechanisms of action.

1. Watchful waiting. Periodic reassessment of symptom level, physical findings, routine laboratory testing and optional urologic diagnostic procedures.

2. Surgery. Best chance for symptom improvement. Highest rate of significant complications. Transurethral resection most common followed by transurethral incision.

3. Balloon Dilation. Fewer complications and less effective than surgery. Temporary with frequent recurrence.

4. Alpha Blockers. Alpha₁-adrenergic receptor blockers such as doxasozin (Cardura), prazosin (Minipress) and terazosin (Hytrin), relax smooth muscle of the bladder neck and prostate. Non-selective alpha blockers have too many side effects.

5. Finasteride (Proscar). 5-alpha reductase inhibitor blocking conversion of testosterone to dihydrotestosterone, the major intraprostatic androgen in men. Reduces the size of the prostate.

Describe the diagnosis and treatment of common sexually transmitted diseases.

1. Chlalmydia: genital swab specimens; doxycycline or azithromycin

2 Gonorrhea: genital swab specimen; ceftriaxone

3. Epididymitis: chlamydia and gonorrhpeae usually; ofloxacin if pathgen not known.

4. PID: Chlamydia or gonorrhoeae et al; cetriaxone and doxycycline

5. Trichomoniasis: wet prep; metronidazole

6. Bacterial vaginosis: wet prep and KOH; metronidazole

7. Vulvovaginal candidiasis: pelvic; miconazole suppositories

8. Syphilis: VDRL, FTA-ABS; penicillin G

9. Chancroid: culture; ceftriaxone

10. Pediculosis and Scabies: microscope exam; permethrin 5%

11. Genital warts: observtion; podophyllin or cryotherapy

12. Genital herpes: Tzanck test; acyclovir