INTERNAL MEDICINE EOR SMARTYPANCE

Vascular Disease

Aortic aneurysm: flank pain, hypotension, pulsatile abdominal mass; screen if male >65 and hx of smoking Tx: immediate surgical repair if >5.5cm or expands >0.5cm per year; monitor annual if >3cm, q6mo >4cm; beta-blocker Aortic dissection: sudden onset tearing chest pain between scapula; diminished pulses; widened mediastinum; unequal blood pressures on the arm Tx: ascending aorta = surgical emergency; descending: beta-blocker Arterial embolism/thrombosis: sudden arterial occlusion Pain, pallor, pulselessness, paresthesia, paralysis, poikilothermia Angiography = gold standard Tx: IV heparin if not limb-threatening call vascular surgeon for angioplasty, graft or endarterectomy Giant cell arteritis: inflammation of large and medium vessels - jaw claudication and HA, thickened temporal artery scalp pain elicited by touching scalp/hairbrush; acute vision disturbances; associated with polymyalgia rheumatica Amaurosis fugax (temporary monocular blindness) secondary to anterior ischemic optic neuritis Dx: ESR >100, temporal artery biopsy Tx: high dose prednisone URGENTLY - don't wait for biopsy results Peripheral artery disease: intermittent claudication, ABI <0.9 s/s: lower extremity hair loss, brittle nails, pallor, cyanosis, hypothermia; ulcers pale to black, PAINFUL, lateral/distal arteriography = gold standard tx: definitive = arterial bypass; medical: antiplatelet, anti-lipid, manage r/f, cilostazol, aspirin, Plavix Phlebitis/Thrombophlebitis: spontaneous / after trauma or IV/PICC lines - dull pain, erythema, induration of vein, palpable cord dx: duplex U/S = gold standard tx: symptomatic: NSAIDs, warm compress Varicose Veins: dilated tortuous superficial veins, venous stasis ulcers, ankle edema, LE pain after sitting/standing tx: leg elevation, compression stockings, vein stripping Venous insufficiency: edema, atrophic shiny skin, brawny induration, stasis dermatitis, brown hyperpigmentation, varicosities, ulcers above the medial malleolus dx: ABI, Trendelenburg tests, U/S tx: sclerotherapy, vein stripping, compression hose Venous thrombosis: unilateral (asymmetrical) swelling of lower extremity Virchow's triad: stasis, trauma, hypercoagulability (OCP, cancer, surgery, factor V Leiden) dx: d-dimer, venous duplex U/S = 1st line; venography = gold standard; Homan sign = discomfort behind knee on forced foot dorsiflexion tx: heparin to coumadin bridge

Atrial fibrillation/flutter

A-fib: Irregularly irregular rhythm with disorganized and irregular atrial activations and an absence of P waves A-flutter: Regular, sawtooth pattern and narrow QRS complex

Rheumatic fever

Although rheumatic fever follows a streptococcal throat infection (strep throat), it is NOT an infection. Rather, it is an inflammatory reaction to the infection Rheumatic fever (RF) is caused by an acute, inflammatory immune response to Group A Strep, with the formation of antistreptolysin antibodies which react with proteins on the synovium, heart muscle, and heart valves Modified Jones Criteria: Diagnosis of the first episode of acute rheumatic fever is based on the modified Jones criteria: 2 major criteria or 1 major and 2 minor criteria are required, along with evidence of preceding GAS infection Major: Carditis Chorea Erythema marginatum Polyarthritis Subcutaneous nodules Minor: Arthralgia Elevated ESR or C-reactive protein Fever Prolonged PR interval (on ECG) Tx: aspirin / NSAID, steroid, abx Antistreptococcal prophylaxis should be maintained continuously after the initial episode of ARF to prevent recurrences - PENICILLIN GChildren without carditis should receive prophylaxis for 5 yr or up to age 21 (if the patient turns 21 before 5 yr of prophylaxis is completed)Children with carditis without evidence of residual heart damage receive prophylaxis for 10 yrChildren with carditis and evidence of residual heart damage should receive prophylaxis for > 10 yr; many experts recommend that such patients continue prophylaxis indefinitely

Sick sinus syndrome

Brady-tachy: Arrhythmia in which bradycardia alternates with tachycardia Sinus arrest: prolonged absence of sinus node activity (absent P waves) > 3 seconds

Coronary vascular disease

CAD is the #1 killer in the USA and worldwide ➢ Death rates ↓ yearly since 1968 → MC cause of cardiovascular death and disability Coronary artery disease can be due to either vasospastic disease (Prinzmetal angina) or atherosclerotic disease when a coronary artery narrows due to the build-up of atherosclerotic plaque → characterized by a type of chest pain called angina pectoris → it can be further divided into stable angina, unstable angina, and myocardial infarction RF: smoking, diabetes, dyslipidemia (↑ LDL, ↓ HDL), hypertension, family hx, men > 55, women > 65 Dx: high-sensitivity high CRP, lipids, triglycerides, carotid U/S Tx: Smoking cessation, lifestyle (BP, LDL/HDL, obesity) Primary prevention = platelet inhibitors (Aspirin, etc.) = cornerstone Secondary prevention = aspirin, β-blockers, ACE-I/ARB, statins; nitro if symptomatic MOA of atherosclerotic disease: Foam cells are macrophages that gobble up lipids in the wall; it then dies off and stays there and becomes a foam cell; when it dies it releases cytokines that attract more macrophages to the area ⇒ plaque clot Fibrous plaque forms over lipid core: Complete clot - ST-elevation MI; Incomplete clot - unstable angina/NSTEMIVulnerable plaque is easy to rupture; thick plaque is stableAdhesion, activation, aggregation, propagation of clot, platelet adherence

Chronic Bronchitis

Defined as a chronic cough that is productive of phlegm occurring on most days for 3 months of the year for 2 or more consecutive years without an otherwise-defined acute cause Exposure to irritants (e.g. cigarette smoke) → hypertrophy/hyperplasia of bronchial mucous glands, goblet cells in bronchioles, cilia less mobile → increased mucus production, less movement → mucus plugs → obstruction in bronchioles → air-trapping → productive cough Rales (crackles), rhonchi, wheezing, signs of cor pulmonale (peripheral edema, cyanosis) ABGs: Respiratory acidosis (arterial PCO2> 45 mmHg, bicarbonate > 30 mEq/L) PFT's: FEV1/FVC ratio of less than 0.7Increased TLC (air trapping) Chest radiograph: peribronchial and perivascular markings ↑ HGB and HCT are common because of the chronic hypoxic state Pulmonary HTN with RVH, distended neck veins, hepatomegaly Obese and cyanotic = blue bloaters Diagnostic Studies: PFTs/spirometry = gold standard diagnosis COPDFEV1 = important factor of prognosis and mortality (< 1 L = increased mortality)Obstruction: decreased FEV1, decreased FVC, decreased FEV1/FVC; Hyperinflation: increased lung volumes: increased RV, TLC, RV/TLC, increased FRC (functional residual capacity) CXR/CT scanEmphysema: hyperinflation: flat diaphragm, increased AP diameter, decreased vascular markings; bullaeChronic bronchitis: increased AP diameter, increased vascular markings, enlarged right heart border ECG: cor pulmonale: RVH, RAE, RAD, R-sided heart failure (due to longstanding pulmonary hypertension), MAT, hypertension Clinical Therapeutics: Smoking cessation = single most important step Bronchodilators: combo therapy β2 agonist + anticholinergic = greater response than used alone - tx of choice in stable COPD with resp. symptomsShort-acting (SAMA) or long-acting (LAMA) muscarinic agent (also known as an anticholinergic agent): tiotropium (Spiriva) inhaled long-acting; ipratropium (Atrovent)Ipratropium preferred over short-acting B2 agonist in COPDs/e: dry mouth, thirst, blurred vision, urinary retention, difficulty swallowing, mydriasisContraindications: glaucoma, BPHShort-acting (SABA) or long-acting (LABA) beta 2 agonists: albuterol, terbutaline, salmeterol (long-acting)s/e: B1 cross-reactivity, tachycardia/arrhythmias, muscle tremor, CNS stimulationContraindications: severe CAD; caution in pt. with DM (hyperglycemia), hyperthyroidTheophylline: only used in refractory cases bc narrow therapeutic index - monitor serum levels to prevent nausea, palpitations, arrhythmias, seizures from toxic levels; higher doses needed in smokers and coffee drinkers- don't initiate in acute exacerbation +/- inhaled glucocorticoids: inhaled corticosteroids not considered monotherapys/e: osteoporosis, thrush Oxygen: only medical therapy proven to decrease mortality (decreases pulmonary hypertension/cor pulmonale by decreasing hypoxia-mediated pulmonary vasoconstriction)Long-term oxygen therapy in all patients with COPD who have chronic hypoxemia defined as resting PaO2 < 55 mmHg or SaO2 <89% Health Maintenance: Control triggers: pollutants, bronchospasm, cardiopulmonary disease, meds (decongestants, B blockers, sedative) Infections: bronchitis and pneumonia Prevention of exacerbations: SMOKING CESSATION Vaccinations: pneumococcal vaccine and influenza vaccine Pulmonary rehab: improves the quality of life, dyspnea, and exercise intolerance Surgery: lung reduction surgery - improves dyspnea by removing damaged lung; lung transplant Azithromycin has anti-inflammatory properties in the lung

Valvular heart disease

Diastolic Murmur: almost always mean heart disease Early = regurgitative flow through an incompetent valve (usually aortic) Rumbling = mid/late diastole suggests stenosis of AV valve (usually mitral)Aortic regurgitation: soft, high pitched, blowing diastolic along LSB with pt sitting, leaning forward after exhalingMitral stenosis: diastolic low pitched decrescendo and rumbling with opening snap at apexPulmonary regurgitation: high pitch, decrescendo murmur at LUSB, increases with inspirationTricuspid stenosis: mid-diastolic rumbling at LLSB with opening snap Midsystolic Murmurs: aka ejection murmurs; MC kind of heart murmur; peak near mid systole and stop before S2; gap between murmur and S2 pathologic - secondary to structural cardiovascular abnormalities physiologic - secondary to physiologic alteration in body innocent - not associated with detectible physiologic/structural abnormality Aortic stenosis: systolic ejection crescendo-decrescendo RUSB Pulmonic stenosis: hard midsystolic ejection crescendo-decrescendo murmur with widely split S2 at LSB that radiates to left shoulder and neck HCOM: medium-pitched, mid-systolic murmur that decreases with squatting and increases with strainingS4 gallop and apical lift with a thick, stiff left ventricle Mitral valve prolapse: midsystolic ejection click at the apex Pansystolic (holosystolic) murmurs - pathologic; heard when blood flows from high to low-pressure chamber; begins immediately with S1 and continues up to S2 Mitral regurgitation: blowing holosystolic murmur at the apex with a split S2 Tricuspid regurgitation: high pitched holosystolic murmur at mid-LSB Ventricular septal defect: harsh holosystolic murmur heard at LSB with wide radiation and fixed, split S2

Diverticular disease

Diverticulitis will present as → a 67-year-old man with a long history of constipation presents with steady left lower quadrant pain. Physical exam reveals low-grade fever, mid-abdominal distention, and lower left quadrant tenderness. Stool guaiac is negative. An absolute neutrophilic leukocytosis and a shift to the left are noted on the CBC. Diverticulosis will present as → a 63-year-old male who is being evaluated in the emergency department for an episode of painless bright red blood per rectum for two hours. Inflammation of an abnormal pouch (diverticulum) in the intestinal wall, usually found in the large intestine The presence of the pouches themselves is called diverticulosis. When they become inflamed, the condition is known as diverticulitis. Left-sided Appy Most common location: Sigmoid colon Fever/chills/Nausea/vomiting/left-sided abdominal pain DX: Abdominal/Pelvic CT scan revealing fat stranding and bowel wall thickening The most common cause of massive lower gastrointestinal bleeding Treatment = Ciprofloxacin or Augmentin/ + Metronidazole (Flagyl) Recurrent attacks or the presence of perforation, fistula, or abscess require surgical removal of the involved portion of the colon. Treat by increasing the bulk in the diet with high-fiber foods and bulk additives such as Metamucil

Emphysema

Exposure to irritants (e.g. cigarette smoke) → degrades elastin in alveoli, airways → lose elasticity → low pressure during expiration pulls walls of alveoli inward → collapse → air-trapping distal to collapse → septa breaks down → neighboring alveoli coalesce into larger air spaces → decreased surface area available for gas exchangeLoss of elastin → lungs more compliant (lungs expand, hold air)Alveolar air sacs permanently enlarge, lose elasticity → exhaling is difficult DOE = hallmark symptom Hyperinflation of lungs + hyperresonance to percussion decreased/absent breath sounds, decreased fremitus, barrel chest (increased AP diameter), quiet chest, pursed-lip breathingIndividuals are able to oxygenate blood (pink) but they have to purse their lips to do so (puffers) = Pink Puffers!Pursing lips increases pressure in the airway → keeps the airway from collapsing → weight lossBarrel chest due to air trapping and hyperinflation of lungs CXR reveals loss of lung markings, hyperinflation, increased anterior-posterior diameter PFTs show FVC decreased (esp. FEV1) + increased TLC (due to air trapping) ABG/ labs: respiratory alkalosis, mild hypoxemia, normal CO2 Cachectic with pursed-lip breathing ⇒ "pink puffers"

Hepatitis D

Hepatitis D occurs only when coinfected with Hepatitis B Risk of hepatocellular carcinoma Suspect hepatitis D particularly when cases of hepatitis B are severe or when symptoms of chronic hepatitis B are worsening DX: If serologic tests for hepatitis B confirm infection and clinical manifestations are severe, antibody to HDV (anti-HDV) levels should be measuredAnti-HDV implies active infection. It may not be detectable until weeks after the acute illness. Treat and prevent infection as for hepatitis B.

Hypertensive emergencies

Hypertensive emergency: BP usually >180/120 WITH impending or progressing end-organ damage Hypertensive Urgency: BP usually > 180/120 WITHOUT signs of end-organ damage Malignant HTN: Diastolic reading > 140 associated with papilledema and either encephalopathy or nephropathy Treatment: Hypertensive emergency = sodium nitroprusside (drug of choice) Hypertensive urgency = clonidine (drug of choice) Malignant hypertension = hydralazine

Hypoventilation syndrome

Hypoventilation syndrome may be secondary to several mechanisms, including central respiratory drive depression (drugs -narcotics, benzodiazepines, neurologic disorders - multiple sclerosis, etc.), neuromuscular disorders (ALS, myasthenia gravis, etc.), chest wall abnormalities, obesity hypoventilation, and COPD Obesity hypoventilation syndrome (OHS), also known as Pickwickian syndrome, is a condition in which severely overweight people fail to breathe rapidly or deeply enough, resulting in low oxygen levels and high blood carbon dioxide (CO2) levels. s/s: sluggish/sleepy during day Sequelae: pulmonary hypertension, cor pulmonale, secondary erythrocytosis DX: PFTs, sleep studies, CXR, arterial blood gas, serum bicarb TX: lifestyle, healthy weight, physical activity, CPAP, tracheostomy Sleep apnea falls into this category

Congestive heart failure

Left ventricular failure will present as → a 60-year old caucasian male with shortness of breath and fatigue on exertion. On physical exam, you note an S3 heart sound, crackles on pulmonary auscultation, and a displaced left apical impulse. He undergoes an echocardiogram and is found to have a dilated left ventricle and an ejection fraction of 35%. MC cause: CAD, HTN, MI, DM - LV remodeling ⇒ dilation, thinning, mitral valve incompetence, RV remodeling Sx: exertional dyspnea ⇒ rest, chronic nonproductive cough, fatigue, orthopnea, nocturnal dyspnea, nocturia Signs: Cheyne-stokes breathing, edema, rales, S4 (diastolic HF, preserved EF); S3 (systolic; reduced EF); JVD >8cm, cyanosis, hepatomegaly, jaundice NY heart failure classification:Class 1: no limitation of physical activityClass 2: slight limitation physical activity; comfortable at restClass 3: marked physical limitation; comfortable at restClass 4: can't carry on physical activity; anginal syndrome at rest Dx: BNP, EKG, CXR (Kerley B lines); echo = gold (best to assess size and function of chambers) Tx: Systolic: ACE-I + B-blocker + loop diuretic Diastolic: ACE-I + B-blocker or CCB

Dilated Cardiomyopathy

MC type; an index event or process (MI) damages myocardium, weakening heart muscle à decreased ventricular contraction strength + dilation left ventricle; systolic heart failure Reduced contraction strength; large heart; caused by ischemia (CAD, MI, arrhythmia) PE: dyspnea, S3 gallop, rales, JVD Tx: no alcohol!!!; ACE-I, diuretic

Myocarditis

Myocarditis is a disease that causes inflammation of the heart muscle (myocardium) Myocarditis is usually caused by a viral infectionetiologies: bacterial, parasitic, cardiotoxin, systemic disorders, radiation, hypersensitivity Symptoms include fatigue, fever, chest discomfort, dyspnea, palpitations, tachycardia disproportionate to fever or discomfortA severe case can weaken the heart, which can lead to heart failure, abnormal heartbeat, and sudden death. Dx: endomyocardial biopsy = gold standard; clinical presentation, cardiovascular MRI; echo = decreased ventricular EF with hypokinesis Tx: supportive, heart failure treatment prn, antidysrhythmic prn

Sinus arrhythmia

Normal, minimal variations in the SA Node's pacing rate in association with the phases of respiration. Heart rate frequently increases with inspiration, decreases with expiration

Premature Beats

PVC: Early wide bizarre QRS, no p wave seen PAC: abnormally shaped P wave PJC: Narrow QRS complex, no p wave or inverted p wave

Cor pulmonale

Patient will present as → 65 y/o with 3 days of progressive dyspnea and purulent sputum production. The patient takes albuterol and tiotropium bromide for moderate COPD. His PMH is relevant for a 40 pack-year smoking history, type II DM, hyperlipidemia, and coronary artery stenting 2 years ago. PE shows barrel-shaped chest, inspiratory crackles, hepatojugular reflux, pulsus paradoxus, and ventricular gallop. His temperature is 38.1°C (100.5°F), his pulse is 130/min, respirations are 28/min, blood pressure is 130/84 mmHg, and pulse oximetry on room air shows an oxygen saturation of 86%. Right ventricular enlargement and eventually failure secondary to lung disorder that causes pulmonary artery HTN Etiology: COPD (most common), pulmonary embolism, vasculitis, asthma, ILD, acute respiratory distress syndrome Physical Exam: Lower extremity edema, neck vein distention, hepatomegaly, parasternal lift, tricuspid/pulmonic insufficiency, loud S2 DX: The diagnosis of cor pulmonale is usually made with an echocardiogram that shows evidence of increased pressure in the pulmonary arteries and right ventricle. Follow up tests can be done to identify the underlying cause, for example, spirometry can be done to look for chronic lung disease The gold standard diagnostic test to directly measure pulmonary pressures and assess for response to vasodilating medications is a right heart catheterization. TX: Diagnose and treat the underlying condition before cardiac structure change becomes irreversible Diuretics not helpful! May be harmful

Gout

Patient will present as → A 54-year-old man presents to your office with a one-day history of acute onset pain of the right knee. The patient states he has had similar episodes in the past in his metatarsophalangeal joints, which were less severe and relieved by ibuprofen. He denies any recent trauma or fever. Pertinent history includes consumption of 4-5 beers per day, sexual activity with multiple female partners over the past year, and two hospitalizations for nephrolithiasis. Physical examination shows a tender, mildly swollen, and erythematous right knee with a limited range of motion. Joint aspiration (image) shows yellow crystals in parallel to the polarization filter, and 24,200 leukocytes /µL (normal <200). Gout involves the accumulation of uric acid in the soft tissue of joints and bone Altered purine metabolism and sodium urate crystal precipitation into the synovial fluid, M>W (9:1) until menopause (1:1) Usually young, >30 yo, asymmetric; great toe; tophi s/s: MC = podagra (attack of MTP of the great toe) (70% of cases); pain, swelling, redness, exquisite tenderness. In chronic gout = tophi Diagnosis is by arthrocentesis - rod-shaped negatively birefringent. Serum uric acid level >8 (not diagnostic) Imaging: small, punched out lesions on XR = high likelihood diagnosis Tx: lifestyle: elevation, rest, decrease purines (meats, beer, seafood, alcohol), weight loss, increase protein, limit alcohol Pharm: NSAIDs = drug of choice (indomethacin tid); colchicine is effective but bad GI side effects. Steroid injections for those who can't take NSAIDs, oral prednisone if other meds not toleratedThiazide diuretics and aspirin should be avoidedManagement between acute attacks = colchicine, allopurinolDon't start someone on allopurinol in an acute attack

Pseudogout

Patient will present as → A 59-year-old woman complaining of severe left hip pain for the past day. She states the hip feels warm and looks enlarged. The patient has had multiple similar episodes in her knees, hips, and wrists over the last few years, for which she took ibuprofen as needed. Past medical history is significant for hypertension and type II diabetes mellitus, which are well managed with lisinopril and metformin, respectively. Vital signs are within normal limits. Physical examination shows an erythematous and swollen left hip joint. It is tender to palpation with decreased active and passive range of motion. Arthrocentesis of the left hip is performed. Gram stain is negative. Polarized light microscopy shows rhomboid-shaped, weakly positively birefringent crystals. Pseudogout; usually >60yo; large joints, lower extremity; no tophi Similar gout symptoms Dx: rhomboid-shaped calcium pyrophosphate crystals - positively birefringentXR shows fine, linear calcifications in cartilage Tx: NSAIDs, colchicine, intra-articular steroid injectionsColchicine = prophylaxis, NSAIDs = acute attacks

Rheumatoid arthritis

Patient will present as → A 63-year-old woman presents with pain in her hands for five years. She describes the pain as progressive - coming on slowly and worsening over the course of the three years. She says that her mother had problems with their hands as well. A hand X-ray is obtained which shows soft tissue swelling and marked juxta-articular osteopenia in her metacarpophalangeal and proximal interphalangeal joints, and minor bony erosions. MORNING JOINT STIFFNESS > 30 minutes after initiating movement and improves later in the day (vs OA which gets worse throughout the day and if morning stiffness is present will be < 30 minutes) Prodrome of constitutional symptoms including fevers, fatigue, weight loss, and anorexia Small joint stiffness (MCP, wrist, PIP, knee, MTP, shoulder, ankle) worse with rest Symmetric arthritis: swollen, tender, and boggy jointBoutonniere deformity: flexion at PIP, hyperextension of DIPSwan neck deformity: flexion at DIP with joint hyperextension at PIPUlnar deviation at MCP jointRheumatoid nodules Diagnostic studies include: (+) Rheumatoid Factor (sensitive but not specific); Increased CRP and ESR (+) Anti-citrullinated peptide antibodies (most specific for RA) Treatment: Prompt initiation of DMARDs: Methotrexate - Methotrexate (MTX) is the cornerstone of therapy for RA and is effective as monotherapy for many patients. Hydroxychloroquine (Plaquenil ) - Hydroxychloroquine (HCQ) may be added to a number of traditional DMARDs, including MTX, to improve response. HCQ is less effective as monotherapy Sulfasalazine - Sulfasalazine (SSZ) is often used in combination with HCQ and MTX as part of the so-called "triple therapy" regimen. When used in this combination, response rates may rival those seen with biologic DMARDs. Leflunomide - LEF is effective as monotherapy for both RA and spondyloarthritis, and therefore may be a good choice when the clinical diagnosis is less clear. Diarrhea is a common side effect, however, and may limit its use. Other - Other drugs with a much more limited role, due to the more effective and/or safer agents that are available, including azathioprine, gold, and cyclosporine NSAIDs for pain control and low dose corticosteroids Biologic agents — The development of biologic agents represented an advance in the treatment of RA comparable to the introduction of glucocorticoids.The cytokines interleukin (IL)-1 and tumor necrosis factor (TNF)-alpha both mediate inflammation and bone resorption in RA. Agents that inhibit B-cell function, T-cell function, and the actions of proinflammatory cytokines (eg, the human recombinant IL-1 receptor antagonist, anakinra, and anti-TNF-alpha agents including etanercept, infliximab, and adalimumab) are all used for the treatment of RA

Gastroenteritis

Patient will present as → a 21-year-old bodybuilder presents with complaints of diarrhea, cramps, and low-grade fever for 24 hours. He has been training for a competition, eating large amounts of protein, including shakes made with raw eggs. He reports three thick green "pea soup" stools with blood in the commode today. He denies nausea or vomiting and tolerates liquids and solids. Examination reveals a well-muscled man in no apparent distress; lungs and heart unremarkable; abdomen, with mildly hyperactive bowel sounds and no tenderness or organomegaly; no evidence of hemorrhoids or anal fissure, no masses, and no stool present for hemoccult. Gastroenteritis is an inflammation of the lining of the intestines caused by a virus, bacteria, or parasites Viral gastroenteritis is the second most common illness in the U.S. The cause is often a norovirus infection Salmonella infection is among the most common causes of bacterial cause of gastroenteritis

Mallory-Weiss tear

Patient will present as → a 21-year-old male with hematemesis. He is brought by his girlfriend who reports that he and his buddies have been out drinking every night last week in celebration of his 21st birthday. He reports having vomited each night, but tonight when he started vomiting, he noticed that there was streaking of blood. Concerned, he decided to come to the emergency department. Tear that occurs in the esophageal mucosa at the junction of the esophagus and stomach caused by severe retching and vomiting and results in severe bleeding. Presentation: History of alcohol intake and an episode of vomiting with blood Caused by forceful vomiting. Associated with alcohol use, upper endoscopy showing superficial longitudinal mucosal erosions Treatment: Supportive. May cauterize or inject epinephrine if needed

Reactive arthritis (Reiter syndrome)

Patient will present as → a 23-year-old male with redness of the eye as well as discharge. He reports that he experiences pain with urination and stiffness and pain in the knee and ankle. With further questioning, he reports a history of gonorrhea infection that was diagnosed and treated approximately 5 weeks ago. He is otherwise healthy. On physical exam, there is conjunctivitis, asymmetric oligoarthritis, and discharge from the urethral meatus. Autoimmune response to infection in another part of the body (Chlamydia +/- gonorrhea MC) ASYMMETRIC inflammatory arthritis CONJUNCTIVITIS, UVEITIS, URETHRITIS, and ARTHRITIS (can't see, can't pee, can't climb a tree!) Most commonly seen in Chlamydia (+/- gonorrhea and GI infections such as salmonella, Shigella, Campylobacter, Yersinia) Diagnosed by a history of infection, clinical exam, positive HLA-B27 (80%) Treatment: NSAIDs are the mainstay of therapy, antibiotics to treat the infection that triggered the disease (Chlamydia)

Acute bronchitis

Patient will present as → a 23-year-old-female with a one-week history of cough productive of whitish sputum. This was preceded one week prior by a URI. She denies chills, night sweats, shortness of breath, or wheeze. Temperature is 99.9°F (37.7°C). Acute Bronchitis Cough > 5 days with or without sputum production, lasts 2-3 weeks Chest discomfort shortness of breath +/- fever Etiology - viruses (most common). Cannot distinguish acute bronchitis from URTI in the first few days Labs not indicated, unless pneumonia suspected (HR >100, RR >24, T >38°C, rales, hypoxemia, mental confusion, or systemic illness) → CXR Treatment: Antibiotics not recommended—mostly viral Symptomatic-based treatment NSAIDs, ASA, Tylenol, and/or ipratropium Cough suppressants—codeine-containing cough meds Bronchodilators (albuterol)

Bronchiectasis

Patient will present as → a 25-year-old cystic fibrosis patient complaining of chronic, frequent coughing productive of yellow and green sputum. She recently recovered from a Pseudomonas spp. pneumonia requiring hospitalization. On physical examination, you notice foul breath, purulent sputum, and hemoptysis along with a CXR demonstrating dilated and thickened airways with "plate-like" atelectasis (scarring). A condition in which the lungs' airways become dilated and damaged, leading to inadequate clearance of mucus in airways Mucus builds up and breeds bacteria, causing frequent infections A common endpoint of disorders that cause chronic airway inflammation (CF, immune defects, recurrent pneumonia, aspiration, tumor)½ of cases are due to cystic fibrosis Symptoms include a daily cough that occurs over months or years and production of copious foul-smelling sputum, frequent respiratory infections DX: CXR = linear "tram track" lung markings, dilated and thickened airways - "plate-like" atelectasis; CT chest = gold standard Crackles, wheezes, purulent sputum TX: ambulatory oxygen, aggressive antibiotics for acute exacerbations, CPT (chest physiotherapy = bang on the back); eventual lung transplant

Pericarditis

Patient will present as → a 45-year-old male with type I diabetes mellitus and end-stage renal disease currently on hemodialysis presents to the emergency department with dyspnea, cough and chest pain. He describes the pain as worse during inspiration and when he is lying on his back. Causes: SLE, uremia, coxsackievirus, TB, RA, neoplasm, drug, radiation, scleroderma, MI, open-heart surgery, radiotherapy MOA: inflammation of pericardial sac; often ⇒ pericardial effusion Chest pain that is relieved by sitting and/or leaning forward Pericardial friction rub heard best with patient upright and leaning forward Dressler's syndrome is pericarditis 2-5 days after an acute myocardial infarctions Pericardial friction rub (listen and learn) 00:00 00:03 Maneuver: Sitting leaning forward Position: Erb's-Point (middle left sternal border) Chest Piece: Diaphragm DX: EKG will demonstrate diffuse, ST-segment elevations in the precordial leads Echo may show pericardial effusion/tamponade Tx: Treat underlying disease! NSAIDs 7-14 days; steroids if sx > 48 hrs; abx to treat bacterial endocarditis; pericardiocentesis; head at 45 degrees Dressler's syndrome: pericarditis 2-5 days after acute MI

Diabetes insipidus

Patient will present as → a 25-year-old male complaining of an unabated thirst that began three weeks ago. He is constantly drinking and goes to the bathroom around five times a night. He has lost five pounds over the last few weeks. The patient is on lithium for bipolar disorder. His BP is 115/70. The patient's labs are significant for serum Na of 145 mEq/L (normal: 135-145). Urine osmolality is 185 mOsm/kg, and urine specific gravity is 1.004 (normal: 1.012 to 1.030). Diabetes insipidus (DI) is caused by a deficiency of or resistance to vasopressin (ADH), which decreases the kidneys' ability to reabsorb water, resulting in massive polyuria Central diabetes insipidus - Deficiency of ADH from posterior pituitary/hypothalamusNo ADH production most common type: idiopathic, autoimmune destruction of posterior pituitary from head trauma, brain tumor, infection, or sarcoidosis Nephrogenic diabetes insipidus - Lack of reaction to ADHPartial or complete insensitivity to ADH: caused by drugs (Lithium, Amphoterrible), hypercalcemia and hypokalemia affect the kidney's ability to concentrate urine, acute tubular necrosis DX: Serum osmolality (concentration) is high (unable to stop the secretion of water into the kidneys so blood becomes more concentrated) and urine osmolality is low because it is so dilute Water deprivation test - simplest/most reliable method - continued production of dilute urine despite water deprivation Desmopressin stimulation test:Central: reduction in urine output indicating a response to ADHNephrogenic: continued production of dilute urine (no response to ADH) because kidneys can't respond TX: Central = desmopressin/DDAVP Nephrogenic = sodium and protein restriction, HCTZ, indomethacin

Addison's disease

Patient will present as → a 25-year-old male presents complaining of fatigue, weight loss, and recurrent nausea and vomiting. On physical exam, he appears weak and has skin that appears abnormally tan. Her blood pressure is 90/70. A basic metabolic panel reveals hyponatremia and hyperkalemia Typically autoimmune. May be due to Tuberculosis in endemic areas Destruction of the adrenal cortex resulting in loss of cortisol production (↓ cortisol) Nonspecific symptoms: Hyperpigmentation, hypotension, fatigue, myalgias, GI complaints, weight loss Lab Findings: ↓ sodium, ↓ 8 AM cortisol, ↑ ACTH (primary), ↑ potassium (primary), low DHEA Diagnosis: High dose cosyntropin (synthetic ACTH) stimulation test Blood or urine cortisol is measured after an IM injection of cosyntropin (synthetic ACTH)The normal response is a rise in blood and urine cortisol levels after synthetic ACTH is givenPrimary adrenal insufficiency results in little or no increase in cortisol levels (< 20 mcg/dL) after ACTH is given Treatment: Hydrocortisone/prednisone PO daily Crisis: Hypotension, altered mental statusTreatment: Emergent IV saline, glucose, steroids

Acromegaly

Patient will present as → a 25-year-old man concerned about some "bizarre symptoms" that he has been. He tells you that approximately 6 months ago, he began to experience the following symptoms: headaches, visual defects, weight gain, an appearance of his forehead growing, enlarging hands and feet (he could no longer get his gloves and shoes on), and increased sweating. On examination, mental status is normal, and the apical impulse is felt in the fifth intercostal space, midclavicular line. His blood pressure is 170/ 105 mm Hg. He does have a protruding brow, and three discrete visual field defects are noted (two in the left eye and one in the right eye). His tongue appears enlarged, and he is sweating profusely. Acromegaly and gigantism are usually caused by a pituitary adenoma that secretes excessive amounts of Growth Hormone; rarely, they are caused by non-pituitary tumors that secrete GHRH Gigantism occurs if growth hormone (GH) hypersecretion begins in childhood, before the closure of the epiphyses Acromegaly involves growth hormone GH hypersecretion beginning in adulthood; a variety of bony and soft tissue abnormalities develop Presentation: Large hands, feet, nose, lips, ears, jaw, tongue Presents as gigantism (excessive height) if occurs before epiphyseal closure Diagnosis: GH test 2 hour after glucose load Increased IGF-1 MRI/CT shows a pituitary tumor Treatment: Pituitary tumor removal

Sarcoidosis

Patient will present as → a 30-year-old African American female with a cough, fever, and generalized body aches. You order a CXR which shows bilateral hilar adenopathy. Chronic autoimmune inflammatory disease in which small nodules (granulomas) develop in lungs, lymph nodes, and other organs↑ ACE levels + Bilateral hilar adenopathy Pulmonary manifestations (most common); skin = 2nd most; skin and lymph = most common areas Symptoms vary, depending on the organs affected - fever, weight loss, arthralgias, erythema nodosum = initial presenting sxLupus pernio (chronic, violaceous, raise plaques and nodules commonly found on cheeks, nose, eyes) = pathognomonic for sarcoid and most specific physical exam finding DX: Chest radiograph: Bilateral hilar lymphadenopathy. Reticular infiltrates Hypercalcemia; ACE levels 4x normal, elevated ESR Biopsy of peripheral lesions or fiber optic bronchoscopy for central pulmonary lesionsBiopsy = non-caseating granulomas TX: Steroids = 90% respond to steroid Methotrexate, other immunosuppressive meds Serial PFTs to assess disease progression/guide treatment ACE-I for periodic HTN Prognosis depends on disease severity; spontaneous improvement common Pulmonary fibrosis = leading cause of death

Irritable bowel syndrome

Patient will present as → a 30-year-old female who presents with alternating constipation, diarrhea, and abdominal pain that is relieved by defecation. She has no nausea, vomiting, weight loss, or blood in her stool. Symptom complex marked by abdominal pain and altered bowel function (typically constipation, diarrhea, or alternating constipation and diarrhea) for which no organic cause can be determined; also called spastic colon According to the Rome IV criteria, IBS is defined as recurrent abdominal pain, on average, at least one day per week in the last three months, associated with two or more of the following criteria: Related to defecation Associated with a change in stool frequency Associated with a change in stool form (appearance) DX of exclusion All labs normal, no mucosal lesions: CBC, renal panel, FOBT, O&P, sed rate, ± flex sig Colonoscopy, barium enema, ultrasound, or CT Endoscopy in patients with persistent symptoms, weight loss/anorexia, bleeding or history of other GI Treatment: Diarrhea - diphenoxylate or loperamide (Imodium) Constipation - Colace, psyllium, cisapride Tegaserod maleate (Zelnorm) is a serotonin agonist introduced for the treatment of IBS Rifaximin (Xifaxan) - antibiotic approved for IBS-D Health maintenance: Avoid dairy products and excessive caffeine, high fiber diet, physical exercise, stress management, and relaxation techniques Comorbid: Depression, anxiety, somatization

Cushing disease

Patient will present as → a 32-year-old woman who comes to the clinic because of new skin markings on her abdomen. Physical exam shows a round face, large purple striae over the abdomen, and several ecchymoses over her trunk, arms, and legs. She describes easy bruising, as well as a significant weakness when she tries to stand up from sitting on the ground. Her 24-hour urine free cortisol is 3 x the upper limit, her late-night serum cortisol is elevated and her plasma ACTH level is < 5 pg/mL. Cushing's syndrome is a collection of signs and symptoms due to prolonged exposure to excess cortisol symptoms from ↑ cortisol secretion. It doesn't specify the cause or source of excess Cushing disease = ACTH secreting pituitary microadenoma usually very small on anterior pituitary; F 3x > M secondary - ↑ cortisol due to ACTH excess, typically caused by a pituitary adenoma - ACTH causes adrenals to secrete cortisol Features: Hypercortisolism (↑ Cortisol) ⇒ obesity (buffalo hump, moon facies, supraclavicular pads), HTN, thirst, polyuria, hypokalemia Proximal muscle weakness, pigmented striae; backache, headache, oligomenorrhea/amenorrhea / ED; emotional lability/psychosis Dx: Confirming high cortisol with a 24 hr urine free cortisol, late-night serum cortisol, and/or low-dose dexamethasone suppression test 24-hour urinary free cortisol is the most reliable index of cortisol secretion Once confirmed, the source of the high cortisol needs to be determined with an ACTH levelA high ACTH level indicates an ACTH dependent cause. A low ACTH level indicates an ACTH independent cause (plasma or serum ACTH < 20 pg/mL suggests adrenal tumor If it is an ACTH dependent cause, an MRI of the brain should be done to look for a pituitary adenoma (Cushing disease). If it is an ACTH independent cause, a CT of adrenals should be done to look for an adrenal mass such as an adenoma Low dose dexamethasone suppression test Give a steroid (dexamethasone) ⇒ failure of steroid to decrease cortisol levels is diagnostic ⇒ proceed next to high dose dexamethasone suppression test ⇒ no suppression = Cushing's syndrome Suppression < 5 ugs/dL excludes Cushing with some certainty Tx: transsphenoidal selective resection of pituitary tumor cures 75-90% Irradiation provides remission in 50-60% 95% 5-year survival

Hepatitis E

Patient will present as → a 33-year-old Caucasian woman who comes to the emergency department because of vomiting and fever. The patient works as a global health nurse and her medical history is relevant for recent travel to India. Upon further questioning, the patient mentions that she is concerned because it has been 9 weeks since her last menstruation. Physical examination shows yellowing of the skin and sclera, right upper quadrant tenderness, and hepatomegaly. Her temperature is 101.3°F, pulse is 98/min, respirations are 14/min, and her blood pressure is 120/70 mmHg. Laboratory studies reveal increased aminotransferase levels and a positive pregnancy test. Pregnant women, 3rd world countries Hepatitis E + mother = high infant mortality Treatment: Supportive. Vaccinate against other viral hepatitis. HIV treatment PRN. Hepatitis C: Direct-acting antiretrovirals target complex of enzymes needed for HCV RNA synthesis

Crohn disease

Patient will present as → a 33-year-old male with watery diarrhea, diffuse abdominal pain, and weight loss over the past three weeks. He has not responded to antibiotics. Crohn's disease is an inflammatory bowel disease (IBD) that causes chronic inflammation of the gastrointestinal tract from mouth to anus Etiology = idiopathic (most likely immune reaction to GI tract flora); MC in Caucasians 15-35 y Presents with abdominal pain, weight loss, diarrhea, and oral mucosal aphthous ulcers. Longer standing disease may have severe anemia, polyarthralgia, and fatigue. Most common site is the terminal ileum Distribution from mouth to anus and will commonly present with thickened bowel wall, cobblestoning and "skip" lesions Linear fissures and cobblestone appearance. Tends to be transmural while UC is limited to the mucosa and submucosa Complications include strictures identified by a STRING SIGN on barium study Obstruction, abscess, fistula, and sinus tracts are common 1-3% cancer risk (low) DX: The diagnosis of Crohn's disease can sometimes be challenging, and a number of tests are often required to assist in making the diagnosis. Even with a full battery of tests, it may not be possible to diagnose Crohn's with complete certainty Rectal exam, stool exam, and culture, CBC, electrolytes, TSH, CT-abdomen Upper GI series with small bowel follow-through⇒ Increased ESR, anemia, nutritional and electrolyte imbalance during exacerbation Colonoscopy is most valuable tool for establishing diagnosis / determining extent / guiding treatment⇒ colonoscopy is approximately 70% effective in diagnosing the disease, with further tests being less effectiveA biopsy will show involvement of the entire bowel wall; granulomas are frequent + Anti-Saccharomyces cerevisiae antibodies (ASCA) and perinuclear antineutrophil cytoplasmic antibody may distinguish Crohn and UC TX: Elemental diet Crohn's: supplement with vitamin B12, folic acid, vitamin DSmoking cessationSurgery not curative in Crohn's; curative in UC Aminosalicylates (sulfasalazine, mesalamine) ⇒ corticosteroids ⇒ immune modifying agents5-aminosalicylates: anti-inflammatory agents; good for flares and remission Oral mesalamine: especially active in terminal small bowel and colon; long-acting works throughout entire small intestine and colon; best for maintenance Topical mesalamine: rectal suppositories and enemas: topical treatment is effective in the distal colon Sulfasalazine: works primarily in the colon; s/e: higher side effect profile with sulfasalazine (hepatitis, pancreatitis, allergic reaction, fever, rash); give folic acid with sulfasalazine Corticosteroids: rapid-acting anti-inflammatory drugs used for acute flares only ⇒ oral and topical; long term risk = osteoporosis, increased infections, weight gain, edema, cataracts Immune modifying drugs: 6-mercaptopurine, azathioprine, and methotrexate = steroid-sparingAnti-TNF drugs: inhibits proinflammatory cytokines (-mab) Initial treatment for uncomplicated Crohn's disease is immunosuppressant therapy. If this is not effective, surgery may be required, especially for complications of perforation, hemorrhage, and toxic colitis. The distinction between Crohn's disease and ulcerative colitis is important as chronic treatment approaches vary. Avoidance of surgery is desired in patients with Crohn's disease due to the natural history of recurrence. Indications for surgery in both Crohn's disease and ulcerative colitis include intractable or fulminant disease, massive hemorrhage, colonic obstruction, cancer prophylaxis, colon dysplasia, or cancer. Indications for surgery specific to ulcerative colitis include toxic megacolon, colonic perforation, or extracolonic disease. Indications for surgery specific to Crohn's disease include stricture and obstruction, refractory fistula, abscess, or perianal disease unresponsive to medical therapy.

Ulcerative colitis

Patient will present as → a 34-year-old female with rectal bleeding and diarrhea for the past week. She has had lower abdominal pain and tenesmus for several months. Ulcerative colitis is an inflammatory bowel disease (IBD) that causes long-lasting inflammation and ulcers (sores) in the digestive tract Ulcerative colitis affects the innermost lining of the large intestine (colon) and rectum Presents with hematochezia and pus-filled diarrhea, fever, tenesmus (feeling of incomplete defecation) anorexia, weight loss Inflammation isolated to colon and confined to mucosa and submucosa (unlike Crohn's not transmural)Most common site is the rectumContinuous lesionsMucosal surface only DX: Diagnosis of ulcerative colitis typically requires colonoscopy to see the ulcers, and take a biopsy Show continuous inflammation starting from rectum and extending proximally with loss of haustral markings and lumen narrowing May elect to limit the extent of the exam (flex sigmoidoscopy) if severe colitis is encountered to minimize the risk of perforation of the colon In addition, radiological imaging may be done with the help of CT scan, MRI, a barium enema Barium enema: Lead pipe appearance (loss of haustral markings) ⇒ may cause toxic megacolon A radiograph may show colonic dilation Laboratory tests should be done to screen for anemia, decreased albumin, and electrolyte abnormalitiesAntibody test: Antineutrophil cytoplasmic antibodies (pANCA)Labs: ↑ WBC, ↑ ESR, ↑ CRP, and anemiaLiver function tests ⇒ elevated alkaline phosphatase and γ-glutamyl transpeptidase levels in patients with major colonic involvement suggest possible primary sclerosing cholangitisTo detect nutritional deficiencies, levels of vitamin D and B 12 should be checked every 1 to 2 yrs. Treatment: Colectomy is curative Medications: Prednisone and mesalamine

Pulmonary nodules

Patient will present as → a 35-year-old female who was found to have a small (2.5 cm) pulmonary lesion on chest radiograph found incidentally after a screening exam for a positive PPD at work. The patient has no significant past medical history and is asymptomatic. Pulmonary nodules: < 3 cm = nodule; >3 cm = mass Found on CXR ⇒ get CTIf suspicious ⇒ biopsy (ill-defined lobular or spiculated suggests cancer)Not suspicious ⇒ < 1 cm monitor at 3 mo, 6 mo, then yearly for 2 yr (calcification, smooth well defined edges = benign) Radiographic characteristics help define the malignant potential of solitary pulmonary nodules Growth rate determined by comparison of previous CXR or CTThe lesion that hasn't grown in > 2 yr = benignDouble from 21-40 days = malignantSmall (< 1 cm) monitor at 3, 6, mo then yearly for 2 yr Calcification suggests benign especially if central, concentric, popcorn Margins that are spiculated or irregular ⇒ CA Diameter < 1.5 cm strongly suggests benign; diameter > 5.3 cm strongly suggests CA Tx: management depends on radiographic findings If malignant ⇒ biopsy!

Fibromyalgia

Patient will present as → a 35-year-old woman who comes to your office with a 1-year history of "aching and hurting all over." She also complains of a chronic headache, difficulty sleeping, and generalized fatigue. When questioned carefully, she describes "muscle areas tender to touch." Although the pain is worse in the back, there really is no place free of pain. She also describes headaches, generalized abdomen pains, and some constipation. Widespread muscular pain, fatigue, muscle tenderness, headaches, poor sleep, and memory problems Most common in middle-aged women May affect 3-10% of population, age 20-50, F > M Associated with hypothyroidism, RA, or sleep apnea Clinical manifestations include diffuse pain that is worse in the morning, extreme fatigue, stiffness, painful, tender joints, and SLEEP DISTURBANCES, symptoms often worsened with physical and psychological stress Diagnosis is usually a process of elimination To diagnose fibromyalgia, the widespread pain index must be greater than seven, and the symptom severity scale must be greater than five for at least three months Biopsy, "moth-eaten" appearance type I muscle fibers, injury to the muscle The treatment for fibromyalgia includes stress reduction, sleep/exercise, antidepressants (amitriptyline, SSRIs, and SNRIs), and anticonvulsants (pregabalin/gabapentin) The FDA has approved three drugs to treat fibromyalgia: the antidepressants duloxetine (Cymbalta) and milnacipran (Savella), plus the anti-seizure medicine pregabalin (Lyrica)

Acute/chronic pancreatitis

Patient will present as → a 37-year-old male complaining of rapid onset of severe mid-epigastric pain with radiation to the back after eating a large meal. The pain lessens when she leans forward or lies in the fetal position. Physical exam shows low-grade fever, epigastric tenderness, diminished bowel sounds, and bruising of the flanks. An abdominal CT scan (seen here) shows localized dilation of the upper duodenum and a small collection of fluid in the left pleural cavity. Pancreatitis is inflammation of the pancreas. It happens when digestive enzymes start digesting the pancreas itself Pancreatitis may start suddenly and last for days, or it can occur over many years Symptoms include upper abdominal pain radiating to the back**, nausea, and vomiting. It has many causes, including gallstones and chronic, heavy alcohol useThe mnemonic GET SMASHHED is useful in recalling the most common causes: Gallstones, Ethanol, Trauma, Steroids, Mumps, Autoimmune disease, Scorpion sting, Hypercalcemia, Hyperlipidemia, ERCP and Drugs. Diagnosis is clinical + elevated lipase and amylase Abdominal CT is the diagnostic test of choice - required to differentiate from necrotic pancreatitis ERCP is the most sensitive for chronic pancreatitis Signs: Grey Turner's sign (flank bruising), Cullen's sign (bruising near umbilicus) Treatment: IV fluids (best), analgesics, bowel rest Complication: pancreatic pseudocyst (a circumscribed collection of fluid rich in pancreatic enzymes, blood, and necrotic tissue) Chronic Pancreatitis - the classic triad of pancreatic calcification (plain abdominal x-ray), steatorrhea (high fecal fat), and diabetes mellitus Alcohol abuse Treatment: No alcohol, low-fat diet

Hepatitis B

Patient will present as → a 37-year-old male presents to the occupational health clinic after a needlestick exposure in a patient with cirrhosis. In addition to a standard bloodborne pathogen laboratory panel sent for all needlestick exposures at his hospital, additional hepatitis panels are ordered. The patient's results are shown below: HIV 4th generation Ag/Ab: Negative/NegativeHepatitis B surface antigen (HBsAg): NegativeHepatitis C antibody: NegativeAnti-hepatitis B surface antibody (HBsAb): PositiveAnti-hepatitis B core IgM antibody (HBc IgM): NegativeAnti-hepatitis B core IgG antibody (HBc IgG): Positive Acute and Chronic Transmission: Sexual or sanguineous Serology: HBeAg - highly infectious HBsAg - ongoing infection Anti-HBc - had/have infectionIgM - acuteIgG - not acute Anti-HBs - immune Risk of hepatocellular carcinoma The vaccine is given to all infants (birth, 1-2 mo, 6-18 mo)

Gastritis

Patient will present as → a 37-year-old male with a history of daily NSAID use complaining of epigastric pain, nausea, vomiting, all worsened by eating. On physical examination, he is tender to palpation in the epigastrium. He admits to drinking approximately two beers per day. Dyspepsia (belching, bloating, distension, and heartburn) and abdominal pain are common indicators of gastritis Three causes: 1. Infection - H. pylori (most common) Location: antrum and body Studies: urea breath test or fecal antigen 2. Inflammation of the stomach lining (NSAIDS and Alcohol) NSAIDs: cause gastric injury by diminishing local prostaglandin production in the stomach and duodenum Alcohol: a leading cause of gastritis 3. Autoimmune or hypersensitivity reaction (e.g. pernicious anemia) Location: Body of the fundus Pernicious anemia: + schilling test + ↓ intrinsic factor and parietal cell antibodies Treatment and diagnosis: stop NSAIDs, empiric therapy with acid suppression 4-8 wk of PPI If no response, consider upper GI endoscopy with biopsy and ultrasound Test for H. pylori infection → if H. pylori (+) treat with (CAP) - clarithromycin + amoxicillin +/- metronidazole + PPI (i.e. Omeprazole) Quadruple therapy (PPI, Pepto, and 2 antibiotics) for one week

Hepatitis A

Patient will present as → a 38-year-old female who has just returned from a 2-week trip to Mexico. She complains of nausea, vomiting, loss of appetite, and right upper quadrant abdominal pain. She has been sick for the past 3 days. She complains of passing dark-colored urine for the past 2 days. She has had no exposure to blood products, has no history of intravenous drug use, and has no significant risk factors for sexually transmitted disease. On examination, she looks acutely ill. Her pulse is 100 beats/minute, blood pressure 110/70 mm Hg, respirations 18, and temperature 101°F. Her sclerae are icteric, and her liver edge is tender. Acute - fatigue malaise, nausea, vomiting, anorexia, fever, and right upper quadrant pain. Transmission: Fecal-oral DX: Serum IgM anti-HAVThe IgG antibody to HAV (IgG anti-HAV) test is done to help distinguish acute from prior infection. A positive IgG anti-HAV suggests prior HAV infection or acquired immunity TX: Supportive care Vaccine: killed (inactivated) - given in two dosesRoutine vaccination beginning at age 1 is recommended for all.Vaccinate people at risk (eg, travelers to endemic areas, laboratory workers), and provide postexposure prophylaxis with standard immune globulin or, for some, vaccination

Systemic sclerosis (scleroderma)

Patient will present as → a 41-year-old woman who comes to the office because of cold, blue hands when she goes out in the cold weather for 4 months. She states over the past year she has also had increased difficulty swallowing food and has developed crops of red skin spots. Examination shows that this skin of her hands is thickened, and tightened with the deposition of calcific nodules. There are also multiple telangiectases on the skin of her face. Her laboratories demonstrate the presence of anti-centromere antibodies. Systemic connective tissue disorder causing thickened skin (sclerodactyly), lung, heart, kidney, and GI tract Tight, shiny, thickened skin due to fibrous collagen buildup Limited cutaneous systemic sclerosis "CREST SYNDROME" - Calcinosis cutis, Raynaud's phenomenon, esophageal motility disorder, sclerodactyly (claw hand), telangiectasiaaffects the face, neck as well as distal to the elbow and kneesRaynaud's phenomenon (60-70%) - worsens with smoking, gold, emotional stress. CCBs are the treatment of choice Diffuse cutaneous systemic sclerosis - skin thickening of the trunk and proximal extremities Laboratory studies specific to scleroderma (+) ANTI-CENTROMERE AB: associated with limited crest disease and better prognosis (+) ANTI-SCL-70 AB: associated with diffuse disease and multiple organ involvement (+) ANA Acute management with DMARDs and steroids Treat Raynaud's with vasodilators (CCBs and prostacyclin)

Fatty Liver Disease

Patient will present as → a 43-year-old obese woman with a history of diabetes presents for a routine visit. She denies having any complaints. On physical exam, her physician notices mild hepatomegaly without tenderness to palpation. A liver enzyme panel is sent and reveals elevated transaminases. She is sent for a hepatic ultrasound to evaluate for nonalcoholic fatty liver disease or steatohepatitis. Risk factors: Obesity, hyperlipidemia, insulin resistance DX: Liver function panel: ALT > AST, elevated alkaline phosphatase, viral hepatitis panel to exclude viral cause of chronic hepatitisUltrasound of liver for all patients - findings steatohepatitis (increased echogenicity and coarsened echotexture of the liver)Liver biopsy: Large fat droplets (macrovesicular fatty infiltrates) TX: lifestyle modification - weight loss, alcohol cessation, diabetes control, low-fat diet

Pulmonary hypertension

Patient will present as → a 43-year-old woman with a history of COPD presents to the office with worsening dyspnea, especially at rest. She also complains of dull, retrosternal chest pain. On examination, she has persistent widened splitting of S2. Radiographic findings (seen here) demonstrate peripheral "pruning" of the large pulmonary arteries. Blood pressure in the lungs is usually very low 15/5. In pulmonary hypertension, the pressure increases > 20 mmHg at rest Usually caused by an underlying disorder (constrictive pericarditis, mitral stenosis = MC, LV failure, mediastinal disease compression pulmonary veins)Mitral stenosis: mitral valve = tight so blood can't pass into left ventricle ⇒ pressure backs up to lungs When the right heart can't pump against vascular resistance ⇒ right heart failure = Cor pulmonale Presentation: Dyspnea on exertion, fatigue, chest pain, edema Physical Exam: Loud pulmonic component of second heart sound (P2); Jugular venous distension; Ascites; Hepatojugular reflux; Lower limb edema Diagnose with a right heart catheterization (gold standard) → most accurate measure of pressures CXREnlarged pulmonary arteriesLung fields may or may not be clear, dependent on the underlying cause EchocardiogramIncreased pressure in pulmonary arteries, right ventricles → dilated pulmonary arteryDilatation/hypertrophy of right atrium, right ventricleLarge right ventricle → bulging septum ECG → Right heart strain pattern: T wave inversion in right precordial (V1-V4), and inferior leads (II, III, aVF) TX: identify and treat the underlying cause Pulmonary hypertension secondary to left ventricular failure → optimize left ventricular functionDiuretics (cautiously—individuals may be preload dependent)DigoxinAnticoagulants Cardiogenic pulmonary arterial hypertensionRelax smooth muscle (promote vasodilation), reduce vascular remodeling, improve exercise capacity with prostanoids, phosphodiesterase inhibitors, endothelin antagonists Pulmonary arterial hypertensionEndothelin receptor antagonistsProstanoids

Systemic lupus erythematosus

Patient will present as → a 44-year-old female with intermittent joint pain. The joint pain began about 13 months ago affecting primarily the joints in her hands, wrists, and feet. She expresses concern regarding worsening fatigue, muscle aches, and feelings of depression. The physical exam reveals tender, edematous bilateral wrists; painless oral ulcers; and erythematous maculopapular lesions on her face. Triad of joint pain + fever + malar (butterfly rash) - fixed erythematous rash on cheeks and bridge of nose sparing nasolabial folds (+) Anti-nuclear Ab (ANA): ANA best initial test (not specific) (+) Anti-double-stranded DNA and Anti-Smith Ab: 100% specific for SLE (not sensitive) DX: 4 or more of the following 11 criteria met Malar rash (butterfly rash) Discoid rash (chronic, can scar) Photosensitivity (other rashes from sun exposure) Mucosal involvement (ulcers, mouth, and nose) Serositis (pleuritis, pericarditis) Joint arthritis (2 or more) Renal disorders (abnormal urine protein, diffuse glomerulonephritis) Neurologic disorders (seizures, psychosis) Hematologic disorders (anemia, thrombocytopenia, leukopenia) ANA Other antibodies: Anti Smith, Anti-dsDNA, Anti-phospholipid (Anticardiolipin, Lupus anticoagulant, Anti-B2 Glycoprotein) TX: Manage with sun protection, hydroxychloroquine (for skin lesions), NSAIDs, or acetaminophen for arthritis Pulse dose steroids; cytotoxic drugs (methotrexate, cyclophosphamide)

Celiac disease

Patient will present as → a 45 year-old male from Ireland with complaints of diarrhea, steatorrhea, flatulence, weight loss, weakness and abdominal distension. He reports having 3-5 loose stool per day for the last six months. The condition improves when he fasts. Small bowel inflammation from an immune reaction to eating gluten, a protein found in wheat, barley, and rye Symptoms usually occur following the ingestion of gluten-containing food. Also, has extraintestinal manifestations.Diarrhea, steatorrhea, flatulence, weight loss, weakness, and abdominal distention Associated with dermatitis herpetiformis (chronic, itchy skin rash on elbow, knees, butt, scalp) Associated conditions: T1DM, autoimmune hepatitis, autoimmune thyroid DZ, down, turner, Williams syndrome, increased incidence of small bowel lymphoma Diagnosis: IgA anti-endomysial (EMA) and anti-tissue transglutaminase (anti-TTG) antibodies Small bowel biopsy (duodenum) is the gold standard Treatment: Lifelong gluten-free diet

Peptic Ulcer Disease

Patient will present as → a 45-year-old female presents with burning epigastric pain that starts 2-3 hours after meals. The pain is relieved by food and antacids. Peptic ulcer disease refers to painful sores or ulcers in the lining of the stomach or the first part of the small intestine, the duodenum Etiology: H. pylori, NSAIDs, Zollinger Ellison syndrome (suspect GI malignancy in nonhealing GU-ZES and gastric cancer) Epigastric pain, nocturnal symptoms Duodenal ulcer (food classically relieves pain think Duodenum = Decreased pain with food) Gastric ulcer (food classically causes pain) DX: Endoscopy is the definitive study = gold standard / most accurate diagnostic test → biopsy to r/o malignancyAlarm sx: >50 yo, dyspepsia, history of UG, anorexia, wt loss, anemia, dysphagia Upper GI series: all gastric ulcers seen on UGI series should be followed with endoscopy to r/o malignancy H. pylori testing:Endoscopy with biopsy = gold standard + rapid urease testUrea breath test to confirm eradication after therapyH. pylori stool antigen = > 90 % specific - confirm eradication after therapySerologic antibodies: confirm infection not eradication Complications: bleeding (melena, hematemesis, dizziness), perforation (sudden onset severe, diffuse abdominal pain, rigid abdomen, rebound tenderness), penetration (pain radiating to back), obstruction (vomiting) TX: D/C aspirin/NSAIDs, no alcohol, stop smoking and decrease emotional stress, avoid eating before bedtime, decrease coffee intake, weight loss PPI (most effective), H2 blockers Eradicate H. pylori with "CAP" - clarithromycin, amoxicillin and PPI Surgery for refractory cases

Polyarteritis nodosa

Patient will present as → a 45-year-old male with generalized symptoms such as malaise, fever, sore throat, and joint and muscle aches and pains. He also complains of numbness, tingling, sensory disturbances, and weakness. On physical examination, you notice the presence of tender lumps under the skin, especially on the thighs and lower legs. Laboratory testing is notable for a newly elevated creatinine of 2.6 mg/dL, erythrocyte sedimentation rate, and C-reactive protein. He is also seropositive for hepatitis B virus, ANCA-negative, and guaiac positive. Polyarteritis nodosa (PAN) is a blood vessel disease characterized by inflammation of small and medium-sized arteries (vasculitis), which can restrict blood flow and damage vital organs and tissues Most common in middle-aged men in their 40-50's Associated with Hepatitis B and C - Increased microaneurysms with aneurysmal rupture leading to hemorrhage and thrombosis as well as organ ischemia or infarction Damage to affected artery ⇒ hypertension, aneurysm, thrombosis, necrosisRenal: HTN 2/2 increased renin production (may progress to renal failure)Constitutional: fevers, myalgias, arthritisCNS: neuropathy, amaurosis fugax, peripheral neuropathyDermatologic: livedo reticularis, purpura, ulcers, gangrene Diagnosis requires confirmation with either a tissue biopsy or angiogram Biopsy of an affected artery (gold standard) demonstrates necrotizing arteritis ⇒ or arteriography showing the typical aneurysms in medium-sized arteries ↑ ESR, Most common in middle age men of 45 years old Classic PAN is ANCA negative (P-ANCA positive in < 20% of cases) Renal or mesenteric angiography: microaneurysms with abrupt cut-offs of small arteries) TX: Steroids (prednisone) +/- cyclophosphamide if refractory Plasmapheresis in patients with Hepatitis B virus

Cholelithiasis

Patient will present as → a 45-year-old woman who presents with a chief complaint of recurrent right upper quadrant pain. She reports 30-minute episodes of abdominal pain after eating meals, especially with fast food meals. She has not had any fevers or chills, and her episodes always resolve. Her past medical history includes hyperlipidemia, morbid obesity, and polycystic ovarian syndrome, for which she takes oral contraceptives. You order a right upper quadrant ultrasound, which shows gallstones without any wall thickening.You recommend conservative measures for now, including dietary changes. Cholelithiasis - A precursor to cholecystitis → stones in the gallbladder, pain secondary to contraction of gall against the obstructed cystic duct Asymptomatic (most), symptoms only last few hours Biliary colic—RUQ pain or epigastric Pain after eating and at night Boas sign—referred right subscapular pain RUQ ultrasound - high sensitivity and specificity if >2 mm. CT scan and MRI TX: Asymptomatic—no treatment necessary Elective cholecystectomy for recurrent bouts

Polymyositis

Patient will present as → a 47-year-old female with a complaint of feeling unusually tired and weak. She works as a hairstylist and in the past few weeks has experienced difficulty performing her job. She finds it difficult to work while she has her arms raised. She denies any fevers, weight gain or loss, or any other motor deficits. Physical exam reveals decreased strength in her shoulders. No rash is appreciated. Laboratory evaluation reveals increased creatinine phosphokinase, positive antinuclear antibody, and positive anti-JO 1 antibodies. She is started on high-dose corticosteroids. Polymyositis is a chronic, idiopathic inflammatory DISEASE OF THE MUSCLE causing symmetrical, proximal, PAINLESS (versus polymyalgia rheumatica) muscle weakness i.e. quadriceps femoris Different from dermatomyositis which is characterized by inflammatory and degenerative changes in the skin and muscles Differentiate from Polymyalgia Rheumatica (PMR) by lack of pain which causes stiff joints usually of the shoulder, hip, and neck Diagnosis of PM/DM involves a physical examination of muscle strength, blood tests for muscle enzymes, electrical tests of muscle and nerves, and is confirmed by muscle biopsy ↑ Muscle enzymes: ↑ aldolase, creatine kinase; ↑ ESR, (+) muscle biopsy, abnormal EMG (+) ANTI-JO 1 Ab: Myositis-specific Antibody-associated with interstitial lung fibrosis"mechanical hands" hyperkeratotic cracked hands with a dirty appearance (+) Anti-SRP Ab: signal recognition particle Ab (+) Anti-Mi-2 Ab: specific for dermatomyositis Muscle biopsy: endomysial involvement with PM TX: corticosteroids and sometimes other immunosuppressants (methotrexate/azathioprine)

Anal fissure/fistula

Patient will present as → a 47-year-old man with severe rectal pain when he defecates. He has a fever of 102.2 F (39 C). On exam there is perianal swelling, redness and tenderness. A palpable mass is felt at the anal verge as seen here. Anorectal fistula is an open tract between two epithelium-lined areas and is associated with deeper anorectal abscesses Fistulae will produce anal discharge and pain when the tract becomes occluded. Fistula must be treated surgically Anal fissure Tearing rectal pain and bleeding which occurs with or shortly after defecation, bright red blood on toilet paper Superficial laceration (paper cut like) Pain lasts for several hours and subsides until the next bowel movement Treatment: Sitz baths, increase dietary fiber, and water intake, stool softeners or laxatives Usually heals in 6 weeks Botulinum toxin A injection (if failed conservative treatment)

Cholecystitis

Patient will present as → a 49-year-old female with a 2-day history of right-upper-quadrant, colicky abdominal pain, as well as nausea and vomiting. Examination shows significant pain with palpation in the right upper quadrant. Laboratory findings include an elevated WBC count, alkaline phosphatase, and bilirubin level. Cholecystitis - Inflammation of the gallbladder; usually associated with gallstones Presentation: 5 Fs: Female, Fat, Forty, Fertile, Fair (+) Murphy's sign (RUQ pain with GB palpation on inspiration) RUQ pain after a high-fat meal Low-grade fever, leukocytosis, jaundice Diagnosis: Ultrasound is the preferred initial imaging - gallbladder wall >3 mm, pericholecystic fluid, gallstones HIDA is the best test (Gold Standard) - when ultrasound is inconclusive CT scan - alternative, more sensitive for perforation, abscess, pancreatitis Labs: ↑ ALK phos and ↑ GGT, ↑ conjugated bilirubin Porcelain gallbladder = chronic cholecystitis Choledocholithiasis = stones in common bile duct - diagnosed with ERCP (gold standard) Treatment: Cholecystectomy (first 24-48 hours)

Asthma

Patient will present as → a 5-year-old boy who is brought to the emergency department by his parents for a cough and shortness of breath. He has a past medical history of eczema and seasonal rhinitis. On physical exam, you note a young boy in respiratory distress taking deep slow breaths to try and catch his breath. He has diminished breath sounds in all lung fields with prolonged, expiratory wheezes. Presentation: Most often young patients present with wheezing and dyspnea often associated with illness, exercise, and allergic triggers Airway inflammation, hyperresponsiveness, and reversible airflow obstruction Diagnosis and monitor with peak flow. PFT's: Greater than 12% increase in FEV1 after bronchodilator therapy FEV1 to FVC ratio < 80% (You would expect the amount of air exhaled during the first second (FEV1) to be the greatest amount In asthma, since there is an obstruction (inflammation) you will have a decreased FEV1 and therefore a reduced FEV1 to FVC ratio Treatment guidelines: Mild Intermittent: Less than 2 times per week or 3-night symptoms per month Step 1: Short-acting beta2 agonist (SABA) PRN Mild Persistent: More than 2 times per week or 3-4 night symptoms per month Step 2: Low-Dose inhaled corticosteroids (ICS) daily Moderate Persistent: Daily symptoms or more than 1 nightly episode per week Step 3: Low-Dose ICS + Long-acting beta2 agonist (LABA) daily Step 4: Medium-Dose ICS +LABA daily Severe Persistent: Symptoms several times per day and nightly Step 5: High-Dose ICS +LABA daily Step 6: High-Dose ICS +LABA +oral steroids daily Acute treatment: Oxygen, nebulized SABA, ipratropium bromide, and oral corticosteroids Making Sense of Forced Vital Capacity Forced expiratory volume (FEV) measures how much air a person can exhale during a forced breath. The amount of air exhaled may be measured during the first (FEV1), second (FEV2), and/or third seconds (FEV3) of the forced breath. Forced vital capacity (FVC) is the total amount of air exhaled during the FEV test You would expect the amount of air exhaled during the first second to be the greatest amount. In asthma, since there is an obstruction (inflammation) you will have a decreased FEV1 and therefore a reduced FEV1 to FVC ratio.

Hepatic cancer

Patient will present as → a 52-year-old female with a history of cirrhosis secondary to long-standing alcohol abuse visits your office to discuss a 15-pound weight loss over the last 6 months. She reports early satiety, jaundice and vague abdominal discomfort. Her ascites, generally stable and small, has worsened in the last 3 weeks. Abdominal pain, weight loss, right upper quadrant mass Etiology: Cirrhosis, Hepatitis B, Hepatitis C, Hepatitis D, Aflatoxin from Aspergillus Tumor Marker: ↑ alpha-fetoprotein and abnormal liver imaging Treatment: Resection, Transplant - Poor prognosis

Cirrhosis

Patient will present as → a 53-year-old alcoholic man comes to the emergency department because of an episode of hematemesis. The patient looks disheveled and is disoriented to time and place. Past medical history includes hepatitis C infection. Abdominal examination shows abdominal distension with a fluid wave and caput medusae. Examination of the extremities shows a bilateral "flapping" tremor, red palms, and bilateral 2+ lower extremity edema. A chronic liver disease characterized by fibrosis, disruption of the liver architecture, and widespread nodules in the liver The most common cause is alcoholic liver disease Second most common cause: chronic hepatitis B and C infections Labs: typically AST > ALT ↑ risk for hepatocellular carcinoma - 10-25% of patients with cirrhosis - monitor AFP Hepatic vein thrombosis (Budd Chiari Syndrome): a triad of abdominal pain, ascites, and hepatomegaly Distortion of liver anatomy causes Portal HTN: decreased blood flow through the liver → hypertension in portal circulation; causes ascites, peripheral edema, splenomegaly, varicosity of veins Ascites - accumulation of fluid in the peritoneal cavity due to portal HTN and hypoalbuminemiaThe most common complication of cirrhosisAbdominal distension, shifting fluid dullness, fluid waveAbdominal ultrasound, diagnostic paracentesis - measure serum albumin gradient Salt restriction and diuretics (furosemide and spironolactone)Paracentesis if tense ascites, SOB, or early satiety Esophageal variceal rupture - dilated submucosal veins, retching or dyspepsia, hypovolemia, hypotension, and tachycardia Hepatorenal syndrome: progressive renal failure in ESLD, secondary to renal hypoperfusion from vasoconstriction - azotemia (elevated BUN), oliguria (low urine output, and hypotension Hepatic encephalopathy: ammonia accumulates and reaches the brain causing ↓ mental function, confusion, poor concentrationAsterixis (flapping tremor) - have patient flex handsDysarthria, delirium, and coma Hepatocellular failure → decreases albumin synthesis and clotting factor synthesisProlonged PT - PTT in severe disease - tx with fresh frozen plasma Presentation: Ascites, pulmonary edema/effusion, esophageal varices, Terry's nails (white nail beds) Skin changes: spider angiomata, palmar erythema, jaundice, scleral icterus, ecchymoses, caput medusae, hyperpigmentation Treatment: avoid alcohol, restrict salt, transplant Monitoring: periodic lab values every 3-4 months (CBC, renal function, electrolytes, LFT, coagulation panel), perform endoscopy for varices Abdominal ultrasound every 6-12 months to screen for hepatocellular carcinoma CT-guided biopsy for hepatocellular carcinoma

Pneumoconiosis

Patient will present as → a 53-year-old man presents to the office complaining of progressive dyspnea over the past few years. History reveals that he has worked in construction for the past 20 years demolishing and refurbishing old buildings. He rarely uses any protective breathing equipment. Physical examination demonstrates an afebrile man in mild respiratory distress with inspiratory crackles. The chest x-ray reveals a reticular linear pattern with basilar predominance, opacities, and honeycombing. (asbestosis) Any fibrosis of the lung tissues with a known cause - usually from prolonged environmental or occupational contact Coal worker's: coal mining; complication = progressive massive fibrosisCXR: small nodular opacities in upper lung fields Silicosis: mining, sandblasting, stone, quarry work; increased risk TB and progression to massive fibrosisCXR: small rounded opacities throughout the lung, hilar lymph nodes may be calcified - "eggshell" calcifications Asbestos: insulation, demolition, shipbuilding, construction; complication = mesotheliomaCXR: interstitial fibrosis, thickened pleura, calcified plaques appear on diaphragms or lateral chest wall Berylliosis: high tech field, nuclear power, ceramics, aerospace, electrical plants, foundries; requires chronic steroidsCXR: diffuse infiltrates and hilar adenopathy S/SX: SOB + nonproductive cough + chronic hypoxia, cor pulmonale DX: CXR: interstitial fibrosis PFTs = reduced lung volumes - restrictive dysfunction and reduced diffusing capacity Tx: primarily supportive ⇒ oxygen, vaccinations (pneumococcal, flu) and rehab Steroids to relieve chronic alveolitis Smoking cessation = synergistically linked to lung cancer

Esophagitis

Patient will present as → a 54-year-old female with odynophagia (painful swallowing), dysphagia and retrosternal chest pain Esophagitis is simply inflammation that may damage tissues of the esophagus. It can be divided into two types: ⇒ Non-infectious Reflux esophagitis: mechanical or functional abnormality of the LES Medication-induced: think NSAIDS or bisphosphonates Eosinophilic: Pt with Asthma symptoms and GERD not responsive to antacids. Allergic, eosinophilic infiltration of the esophageal epithelium.Diagnosed with a biopsyA barium swallow will show a ribbed esophagus and multiple corrugated rings Radiation: radiosensitizing drugs include doxorubicin, bleomycin, cyclophosphamide, cisplatinDysphagia lasting weeks-months after therapyRadiation exposure of 5000 cGy associated with increased risk for stricture Corrosive: Ingestion of alkali or acid from attempted suicide ⇒ Infectious - odynophagia (pain while swallowing food or liquids) is the hallmark sign This occurs mainly in patients with impaired host defenses. Primary agents include Candida albicans, herpes simplex virus, and cytomegalovirus. Symptoms are odynophagia and chest pain Fungal: Infectious Candida: linear yellow-white plaques with odynophagia or pain on swallowing. Tx with Fluconazole 100 mg PO daily Viral:HSV: shallow punched out lesions on EGD, treat with acyclovirCMV: large solitary ulcers or erosions on EGD, treat with ganciclovir EBV, Mycobacterium tuberculosis, and Mycobacterium avium intracellulare are additional infectious causes Diagnosis is by endoscopy, biopsy, double-contrast esophagram, and culture Treat the underlying condition Candida: treat with fluconazole 100 mg PO daily HSV: treat with acyclovir CMV: treat with ganciclovir Corrosive: treat with steroid Eosinophilic: treat by removing foods that incite allergic response, topical steroids via inhaler Medication-induced: to prevent bisphosphonate-related esophagitis treat by drinking pills with at least 4 ounces of water, avoid laying down for at least 30-60 minutes after ingestion

Sjögren syndrome

Patient will present as → a 55-year-old female patient complaining of inability to eat completely due to loss of teeth. Along with that the patient also complains of dryness of mouth, for 1 year, and dryness of eyes for 7-8 years. Extraoral examination showed bilateral parotid gland enlargement present on the right and left side of the parotid region. Sjögren syndrome (SS) is a relatively common chronic, autoimmune, systemic, inflammatory disorder of unknown cause attacking the exocrine glands It is characterized by dryness of the mouth, eyes, and other mucous membranes due to lymphocytic infiltration of the exocrine gland and secondary gland dysfunction Salivary glands - xerostomia (dry mouth) Lacrimal glands - dry eyes (keratoconjunctivitis sicca) Parotid enlargement Diagnosis: ANA (especially anti-SS-A (R0) and anti-SS-B (La) (+) Rheumatoid Factor (RF) (+) Schirmer Test (<5mm lacrimation in 5 min) Treat with artificial tears, pilocarpine (cholinergic) for xerostomia Pilocarpine: a cholinergic drug that increased lacrimation and salivation (side effects include diaphoresis, flushing, sweating, bradycardia, diarrhea, N/V, incontinence and blurred vision) Cevimeline: stimulates muscarinic cholinergic receptors

Idiopathic pulmonary fibrosis

Patient will present as → a 55-year-old female who is a current smoker presents with a 9-month history of respiratory symptoms, including dyspnea on exertion, thoracic pain, and dry cough, which were preceded by a pulmonary infection. On auscultation, you hear inspiratory crackles. Pulmonary function tests (PFTs) show only mild impairment of vital capacity with decreased lung volume and a normal to increased FEV1/FVC ratio. Idiopathic pulmonary fibrosis (IPF) is a type of lung disease that results in scarring (fibrosis) of the lungs for an unknown reason Over time, the scarring gets worse and it becomes hard to take in a deep breath and the lungs cannot take in enough oxygen Etiology unknown; MC of all interstitial lung diseases In order to be considered "idiopathic", you must rule out other common causes such as drugs (amiodarone), and environmental or occupational exposuresnon-idiopathic: smoking, viral infections, environmental (silica, hard metal dust), medication, genetics, XRT, GERD Physical exam: Inspiratory crackles DX: CXR shows fibrosis CT chest: diffuse patchy fibrosis with pleural based honeycombing PFTs = restrictive (decreased lung volume, normal/increased FEV1/FVC ratio) Tx: Few effective treatment options other than a lung transplant corticosteroids, O2

Gastroesophageal reflux disease

Patient will present as → a 55-year-old male with complaints of heartburn, belching, and epigastric pain which is aggravated by drinking coffee, eating fatty foods, and lying down. He says it gets better when he takes antacids. Retrosternal pain/burning shortly after eating worse with carbonation, greasy foods, spicy foods, and laying down Endoscopy with biopsy—the test of choice but not necessary for typical uncomplicated casesIndicated if refractory to treatmentAny patient with symptoms of GERD accompanied by dysphagia, recurrent vomiting, weight loss, hematemesis, anemia, melena, or age > 50 should undergo endoscopy as these are considered high risk for the presence of an upper gastrointestinal malignancy. Upper GI series (barium contrast study)—this is only helpful in identifying complications of GERD (strictures/ulcerations) PH Probe is the gold standard for diagnosis (but usually unnecessary) Treatment: H2 receptor blockers, proton pump inhibitors, diet modification (avoid fatty foods, coffee, alcohol, orange juice, chocolate; avoid large meals before bedtime); sleep with trunk of body elevated; stop smoking Nissen fundoplication: antireflux surgery for severe or resistant cases Complications: Strictures or Barrett's esophagus

Hiatal hernia

Patient will present as → a 55-year-old man who presents to the emergency room for palpitations and shortness of breath. He never had this problem before but notes that this has been progressive since he started heavy weight lifting training. He also notes regurgitation and a feeling of food being stuck before passing. Hiatal (diaphragmatic) hernia involves protrusion of the stomach through the diaphragm via the esophageal hiatus. Type 1: sliding hernia ⇒ GE junction and stomach slide into the mediastinum (MC)Increase reflux, treat like GERD Type 2: rolling hernia ⇒ fundus of the stomach protrudes through diaphragm with GE junction, remaining in its anatomic locationSurgical repair to avoid complications Common symptoms: Epigastric pain Substernal regurgitation and dysphagia Chest palpitations and shortness of breath DX: physical exam / Ultrasound TX: Acid suppression may suffice (type 1) Surgical repair can be used for more serious cases (type 2) - fundoplication

hyperlipidemia

Patient will present as → a 55-year-old obese Caucasian gentleman who arrives at your clinic for a routine check-up after having some blood work done during a routing workplace health screening. He is found to have a total cholesterol level of 430 mg/dL. He complains of calf pain while walking to the convenience store, which only resolves with rest. He states that he has a follow-up appointment with his cardiologist because of some occasional chest pain and abnormalities seen on his EKG. Additionally, you notice that he has well-demarcated yellow deposits around his eyes. Screening guidelines: USPSTF recommends screening for patients with NO evidence of CVD and NO other risk factors should begin at 35 years of age NCEP recommends screening all adults at age 20 years regardless of risk factors FOUR GROUPS MOST LIKELY TO BENEFIT FROM STATIN THERAPY Patients with any form of clinical atherosclerotic cardiovascular disease (ASCVD) Patients with primary LDL-C levels of 190 mg per dL or greater Patients WITH diabetes mellitus, 40 to 75 years of age, with LDL-C levels of 70 to 189 mg per dL Patients WITHOUT diabetes, 40 to 75 years of age, with an estimated 10-year ASCVD risk ≥ 7.5% Treatment Targets: There are no recommendations for or against specific target levels for LDL-C or non-HDL-C in the primary or secondary prevention of ASCVD

Hepatitis C

Patient will present as → a 55-year-old rock musician who comes to the office because he has been feeling increasingly tired for 6 months. He has a history of intravenous drug use and alcohol abuse. He states that he feels quite tired, but otherwise has no complaints. The examination is noncontributory. His laboratory investigations are normal aside from elevated liver enzymes. Chronic Asymptomatic Transmission: IV drug use is most common. Also sexual or sanguineous Screen with testing for anti-HCV antibodies Diagnosis with HCV RNA quantitation Risk of cirrhosis and hepatocellular carcinoma Treatment: antiretrovirals target complex of enzymes needed for HCV RNA synthesis

Chronic obstructive pulmonary disease (COPD)

Patient will present as → a 56 yo female with shortness of breath, as well as a productive cough that has occurred over the past two years for at least three months each year. She is a heavy smoker. Physical exam reveals a respiratory rate of 32, slightly labored breathing, and a temperature of 98.9F. Her SpO2 is 90% while receiving oxygen via nasal cannula at 2 Lpm. (chronic bronchitis) Chronic obstructive pulmonary disease ( COPD ) is a chronic inflammatory lung disease that causes obstructed airflow from the lungs due to loss of elastic recoil and increasing airways resistance Includes emphysema and chronic bronchitis ⇒ both usually coexist with one being more dominant Damage to the lungs from COPD can't be reversed Risk factors:Cigarette smoking/exposure is the most important riskAlpha 1 antitrypsin deficiency = genetic and linked to COPD in patients < 40y/o (protects elastin in lungs from damage by WBCs) 30 pack-year history = low dose chest CT

Cholangitis

Patient will present as → a 58-year-old male with acute onset of abdominal pain associated with fever and shaking chills. The patient is hypotensive and febrile with a temperature of 102.2 ° F. Although he is confused and disoriented, he complains of right upper quadrant pain during palpation of the abdomen. His sclerae are icteric and the skin is jaundiced. Cholangitis is an infection of the biliary tract secondary to obstruction, which leads to biliary stasis and bacterial overgrowth Characterized by pain in the upper-right quadrant of the abdomen, fever, and jaundice Choledocholithiasis accounts for 60% of cases Other causes include pancreatic and biliary neoplasm, postoperative strictures, invasive procedures such as ERCP or PTC, and choledochal cysts Organisms: E. coli, Enterococcus, Klebsiella, Enterobacter Presentation: Charcot's triad: RUQ tenderness, jaundice, fever Reynold's pentad: Charcot's triad + altered mental status and hypotension Diagnostic studies: Initial imaging: Ultrasound Best: ERCP Treatment: Cholangitis is potentially life-threatening and requires emergency treatment Aggressive care and emergent removal of stones, Cipro + metronidazole Antibiotics, fluids, and analgesia. ERCP to remove stones, insert a stent, repair the sphincter Cholecystectomy (performed post-acute) Primary sclerosing cholangitis Jaundice and pruritus Associated with IBD, cholangiocarcinoma, pancreatic cancer, colorectal cancer

Polymyalgia rheumatica

Patient will present as → a 62-year-old female complaining of headaches, muscle pain, and weakness. She has no history of headaches but has now started experiencing them every morning for the past two weeks. She reports feeling very weak and tired in the mornings and cannot even raise her arms to brush her hair. Physical exam shows that she has normal strength and a normal range of movement. Her passive range of motion is limited in all directions and she has difficulty rising out of the exam room chair. The erythrocyte sedimentation rate is elevated. Polymyalgia rheumatica (PMR) is an idiopathic inflammatory condition AFFECTING THE JOINTS causing PAINFUL synovitis, bursitis, and tenosynovitis - aching STIFFNESS of PROXIMAL JOINTS (shoulder, hip, neck) in patients > 50 years old PMR is closely related to giant cell arteritis (temporal arteritis) Joint pain versus muscle pain in polymyositis STIFFNESS versus the weakness of polymyositis ESR is markedly elevated (usually > 50) Temporal arteritis is confirmed by TEMPORAL ARTERY BIOPSY Patients respond quickly to low-dose corticosteroid therapy, which may be required for up to 2 years and slowly tapered Methotrexate may also be used

Esophageal Neoplasms

Patient will present as → a 62-year-old man with a history of alcoholism who complains of difficulty swallowing solids that has progressed to difficulty swallowing liquids. He has smoked 1-2 packs of cigarettes per day for the past 38 years. In addition, he reports occasional bouts of hematemesis and hoarseness, along with progressive weight loss and weakness. Progressive dysphagia to solid foods along with weight loss, reflux, and hematemesis Squamous cell m/c worldwide and adenocarcinoma common in the US Adenocarcinoma: Complication of Barrett's esophagus (screen Barrett's patients every 3-5 years with endoscopy), affects distal (lower) 1/3rd of the esophagus Squamous cell: Associated with smoking and alcohol use Affects proximal (upper) 2/3rds of the esophagus Progressive dysphagia, weight loss, hoarseness Diagnostic studies: Endoscopy + biopsy Treatment: Resection

Esophageal varices

Patient will present as → a 64-year-old man with a history of alcoholism, tobacco use, and hypertension presents to the general surgery clinic where he was referred for further evaluation of blood in his stool. He reports occasional abdominal pain relieved transiently with meals and one episode of painful vomiting. Recently, his stools have been black. Spider angiomas, but no palmar erythema or hepatosplenomegaly are observed on the exam. Dilated veins in the distal esophagus or proximal stomach caused by elevated pressure in the portal venous system, typically from cirrhosis Presentation: Often asymptomatic until hematemesis or Etiology: Portal hypertension (from cirrhosis), Budd-Chiari syndrome (from occlusion of hepatic veins) Treatment: Therapeutic endoscopy - endoscopic banding and IV octreotide, prevent with nonselective beta-blockers Screening is indicated when cirrhosis or portal hypertension is diagnosed When high-risk varices are diagnosed, prophylaxis should be started, and further screening is not necessary Otherwise, screening should be repeated every 2 to 3 years for patients without varices and every 1 to 2 years for patients with small varices

Colon cancer

Patient will present as → a 65-year-old male with several months of weight loss, vague right upper quadrant pain, and thin-caliber stools. His medical history is notable for 50-pack-years of smoking and obesity. On exam, he appears chronically ill and has firm hepatomegaly. His labs reveal a hemoglobin of 10.7 g/dL and mildly elevated ALT and AST. Painless rectal bleeding and a change in bowel habits in a patient 50-80 years of age Apple core lesion on barium enema, adenoma most common type Colon cancer screening for average-risk patients should begin at 45 years and end at 75 years of age Stool tests: Guaiac based fecal occult blood (gFOBT) - once per yearFecal immunochemical test (FIT) - once per yearFIT-DNA test (combines FIT with a test that detects altered DNA in stool) - once every one or three years Flexible sigmoidoscopy - once every 5 years or every 10 years with a FIT every year (serious complications occur in approximately 3.4 per 10,000 procedures) Colonoscopy: once every 10 yearsPerforation of the colon occurs in an estimated 3.8 per 10,000 proceduresSerious complications—including perforation, major bleeding, diverticulitis, severe abdominal pain, and cardiovascular events occur in an estimated 25 per 10,000 procedures CT colonography: once every 5 years (1 additional individual per 1000 would develop cancer in his or her lifetime due to radiation exposure) Tumor Marker: CEA More likely to be malignant: sessile, > 1 cm, villous Less likely to be malignant: Pedunculated, < 1 cm, tubular Treatment: Resect tumors and adjuvant chemotherapy

Pulmonary neoplasm

Patient will present as → a 65-year-old woman with a 40 pack-year history of smoking presents with a 7 kg weight loss over the last 3 months and recent onset of streaks of blood in the sputum. PE reveals a thin, afebrile woman with clubbing of the fingers, an increased anteroposterior diameter, scattered and coarse rhonchi and wheezes over both lung fields, and distant heart sounds. Lung cancer is classified into 2 major categories Small cell lung cancer (SCLC), about 15% of cases (poor prognosis) Non-small cell lung cancer (NSCLC), about 85% of cases, four subtypes include adenocarcinoma, squamous cell carcinoma, large cell carcinoma, and carcinoid tumor ⇒ Small Cell (15% of cases) - 99% smokers, does not respond to surgery and metastases at presentation Location: (central mass), very aggressive Treatment: Combination chemotherapy needed Paraneoplastic syndromes: Cushing's, SIADH ⇒ Non-Small Cell (85% lung cancer cases) Adenocarcinoma - most common (peripheral mass), 35-40% of cases of lung cancerMost commonAssociated with smoking and asbestos exposureLocation: PeripheryParaneoplastic syndrome: Thrombophlebitis Squamous cell (central mass) with hemoptysis, 25-35% of lung cancer casesLocation: centralMay cause hemoptysisParaneoplastic syndrome: hypercalcemiaElevated PTHrp Large cell - fast doubling rates - responds to surgery rare (only 5%)Location: Periphery 60%Paraneoplastic syndrome: Gynecomastia Carcinoid tumor (1-2%): lack glandular and squamous differentiationA tumor arising from neuroendocrine cells → leading to excess secretion of serotonin, histamine, and bradykininGI tract carcinoid tumor may metastasize to lung (CA of appendix = MC; appendix → liver → lung)Presentation: hemoptysis, cough, focal wheezing, recurrent pneumoniaCarcinoid syndrome = cutaneous flushing, diarrhea, wheezing, hypotension (telltale sign)Adenoma = MC type (slow-growing, rare) Treatment: Non-Small Cell can be treated with surgery Treatment depends on staging:Stage 1-2 surgeryStage 3 Chemo then surgeryStage 4 palliativeCarcinoid tumors are treated with surgery Small Cell: CAN NOT be treated with surgery will need chemotherapy Associated manifestations: Superior vena cava syndrome (facial/arm edema and swollen chest wall veins) Pancoast tumor (shoulder pain, Horner's syndrome, brachial plexus compression) Horner's syndrome (unilateral miosis, ptosis, and anhidrosis) Carcinoid syndrome (flushing, diarrhea, and telangiectasia)

Gastric Neoplasms

Patient will present as → a 68-year-old man, who presents to your clinic with complaints of fatigue, loss of appetite, and abdominal pain/fullness. He reports a 15-pound weight loss over the last three months. Vital signs are within normal limits. On exam, you discover a firm, enlarged painless lymph node above the patient's left clavicle. Upon further questioning, the patient reports the node has been present for the past 2 months. His stool is Guaiac positive. Abdominal pain and unexplained weight loss are the most common symptoms along with reduced appetite, anorexia, dyspepsia, early satiety, nausea and vomiting, anemia, melena, guaiac-positive stool. Gastric adenocarcinoma in most cases worldwide Virchow's node (Supraclavicular) (view image) Sister Mary Joseph's node (Umbilical) (view image) DX: upper endoscopy with biopsy; linitis plastica - diffuse thickening of stomach wall d/t cancer infiltration (worst type) Treatment: gastrectomy, XRT, chemo; poor prognosis

Anorectal cancer

Patient will present as → a 69-year-old male who complains of rectal pruritus, bleeding with defecation, and a sensation of incomplete evacuation. A palpable mass is noted on digital rectal examination. Rectal bleeding + tenesmus (a feeling of incomplete emptying after a bowel movement), the most common anorectal cancer is adenocarcinoma Primarily adenocarcinomas. Typically colonoscopy is done: whenever rectal bleeding occurs, even in patients with obvious hemorrhoids or known diverticular disease, coexisting cancer must be ruled out. Treated with wide local surgical excision, radiation with chemotherapy for large tumors with metastases

pneumonia

Patient will present as → a 71-year-old male who was admitted to the acute care hospital two days following a massive CVA with a possible brainstem infarct. Because he was also experiencing secondary respiratory failure, he was intubated and placed on mechanical ventilation. He was subsequently transferred to the neurointensive care unit where he was stabilized. His present vital signs are respiratory rate 14 (ventilator rate), temperature 100.4 F. His SpO2 is 95%. His rating on the Glasgow Coma Scale is 5. Viral: adults ⇒ flu = MC cause; kids ⇒ RSV; comes on fast Dx: CXR = bilateral interstitial infiltrates; rapid antigen testing for flu, RSV nasal swab, cold agglutinin titer negative Tx: flu with Tamiflu (A and B) if sx began <48 hrs; symptomatic tx = beta 2 agonists, fluids, rest Bacterial: fever, dyspnea, tachycardia, tachypnea, cough, +/- sputum Dx: patchy, segmental lobar, multilobar consolidation; blood cultures x2, sputum gram stain Tx: outpatient = doxy, macrolides; inpatient = ceftriaxone + azithromycin/respiratory FQs Fungal: common in immunocompromised pt (AIDs, steroid use, organ transplant) Coccidioides (valley fever); non-remitting cough/bronchitis non-responsive to conventional txFungal inhalation in western states; test with EIA for IgM and IgGTx: fluconazole/itraconazole Pulmonary aspergillosis: usually those with healthy immune systemsTx: fluconazole/itraconazole Cryptococcus: found in soil; can disseminate and ⇒ meningitisLumbar puncture for meningitisTx: amphotericin B Histoplasma capsulatum: pulmonary lesions that are apical and resemble cavitary TB; worsening cough and dyspnea, progression to disabling respiratory dysfunction; no disseminationBird or bat droppings (caves, zoo, bird); Mississippi ohio river valleySigns: mediastinal or hilar LAD (looks like sarcoid)Tx: amp B HIV: PJP (pneumocystis jiroveci) Common in HIV patients with CD4 count <200 XR: diffuse interstitial or bilateral perihilar infiltrates Dx: bronchoalveolar lavage PCR, labs, HIV test; low O2 sat despite supplemental oxygen Tx: Bactrim and steroids; pentamidine for allergy Prophylaxis for high risk pt with CD4 <200 = daily Bactrim CURB65: Estimates mortality of community-acquired pneumonia to help determine inpatient vs. outpatient treatment Confusion, urea > 7, RR > 30, SBP < 90 OR DBP < 60, age > 65 0-1 = low risk, consider home tx 2 = probable admission vs close outpatient management 3-5 admission, manage as severe

Diabetes mellitus type 1

Patient will present as → an 11-y/o girl brought to you by her mother who reports weight loss along with increased thirst and urination. The patient has felt tired and nauseous. On examination her weight is below the 5th percentile, she looks thin, and her skin is pale. her blood pressure is 100/70 and her pulse is 104 bpm. Her respirations are deep at a rate of 28 breaths/minute. Her breath smells fruity. Etiology: Autoimmune- HLA-DR3/4/O antibodies. Islet cell antibodies Presentation of Type I DM: Children Polyuria, polydipsia, polyphagia, fatigue, and weight loss Often first recognized as diabetic ketoacidosis:Symptoms: Fruity breath, nausea, vomiting, dehydrationTreatment: IV regular insulin Treatment of Type I DM: Insulin Dawn Phenomenon: Normal glucose until 2-8 am when it rises. Results from decreased insulin sensitivity and a nightly surge of counter-regulatory hormones during nighttime fasting Treat with bedtime injection of NPH to blunt morning hyperglycemia, avoiding carbohydrate snack late at night Somogyi effect: Nocturnal hypoglycemia followed by rebound hyperglycemia due to a surge in growth hormone Treat with decreased nighttime NPH dose or give bedtime snack Insulin waning: a progressive rise in glucose from bedtime to morning Treat with a change of insulin dose to bedtime DKA: Fruity breath, weight loss, rapid respirations, hypotension Diabetic ketoacidosis (DKA) should always be handled in a hospitalized setting, usually an intensive care unit, and often with an endocrinologist's consultation, if appropriate. TREAT WITH FLUIDS! Patients with DKA are always dehydrated and need large-volume IV fluid resuscitation, usually isotonic fluids such as normal saline. If the corrected serum sodium level is high, this can be reduced to half-normal saline. Insulin should always be administered by an IV pump to guard against accidental overdose. Diagnosis of DM is made by one of the following: Random blood glucose level of > 200 mg/dL + diabetic symptoms 2 separate fasting (8 hours) glucose levels of > 126 mg/dL 2-hour plasma glucose of > 200 on an oral glucose tolerance test (3-hour GTT is the gold standard in GDM) Hemoglobin A1c of > 6.5% Insulin and C-peptide levels - low or inappropriately normal fasting C-peptide and insulin levels with concomitant hyperglycemia High fasting insulin and C-peptide levels suggest T2DM Insulin, GAD65, and IA-2 antibodies - If one or more of the antibodies are present, and especially if two or more are positive, the patient should be presumed to have type 1 diabetes and should be treated with insulin replacement therapy Monitoring/evaluation of glycemic control Hemoglobin A1crepresents mean glucose level from previous 8-12 weeks (approx lifespan of an RBC)useful to gauge the 'big-picture' overall efficacy of glucose control in patients (either Type 1 or Type 2) to assess the need for changes in medication/insulin levelsTreatment goal of A1c < 7.0% "finger-stick" blood glucose monitoringuseful for insulin-dependent (either type 1 or 2) diabetics to monitor their glucose control and adjust insulin doses according to variations in diet or activityTreatment goals: < 130 mg/dL fasting and < 180 mg/dL peak postprandial

Carcinoid tumor (pulmonary)

Patient will present with → a 43-year-old man who comes to the emergency department because of a 3-week history of episodic cutaneous flushing, diarrhea, and wheezing. He has a past medical history of hypertension and type 2 diabetes mellitus. His temperature is 36.6°C (97.9°F), pulse is 125/min, respirations are 30/min, and blood pressure is 90/60 mm Hg. Pulmonary examination shows diffuse wheezes in both lung fields. Cardiac examination shows a prominent "v" wave of the jugular vein and a 1/6 holosystolic murmur best heard on the left lower sternal border. Abdominal examination shows hyperactive bowel sounds. A tumor arising from neuroendocrine cells → leading to excess secretion of serotonin, histamine, and bradykinin Common primary sites include GI (small and large intestines, stomach, pancreas, liver), lungs, ovaries, and thymusThe most common site of a neuroendocrine (carcinoid) tumor to metastasize to is the liverCarcinoid tumor of the appendix is the most common cause. The appendiceal cancer travels from the appendix then to the liver where it metastasizes to the lungs Usually asymptomatic until liver metastasis; symptoms develop occasionallyGI tract tumor→ hormone secretion → enter into enterohepatic circulation → liver inactivates hormones → no symptomsLiver tumor → hormone secretion → released into circulation + liver dysfunction → symptoms Carcinoid syndrome (the hallmark sign) = Cutaneous flushing, diarrhea, wheezing and low blood pressure is actually quite rare and occurs in ~ 5% of carcinoid tumors and becomes manifest when vasoactive substances from the tumors enter the systemic circulation escaping hepatic degradation. The syndrome includes flushing, ↑ intestinal motility (diarrhea), itching and less frequently, heart failure, vomiting, bronchoconstriction, asthma, and wheezing↑ Serotonin leads to collagen fiber thickening, fibrosis = heart valve dysfunction → tricuspid regurgitation, pulmonary stenosis/bronchoconstriction, and wheezing↑ Histamine and bradykinin = vasodilation and flushing↑ serotonin synthesis → ↓ tryptophan → ↓ niacin/B3 synthesis = pellagra DX: CT-Scan to locate the tumors Octreoscan → radiolabeled somatostatin analog (octreotide) binds to somatostatin receptors on tumor cells Urinalysis → elevated 5-hydroxyindoleacetic acid (5-HIAA) → is the main metabolite of serotonin and is used to determine serotonin levels in the body Pellagra (niacin/B3 deficiency) - ↑ serotonin synthesis → ↓ tryptophan → ↓ niacin/B3 synthesis Chest X-Ray shows low-grade CA seen as pedunculated sessile growth in the central bronchi Bronchoscopy- pink/purple central lesion, well-vascularized Treatment is by surgical excision and carries a good prognosis The lesions are resistant to radiation therapy and chemotherapy Octreotide - a somatostatin analog that binds the somatostatin receptors and decreases the secretion of serotonin by the tumor Niacin supplementation

Esophageal strictures

Patient will present with → solid food dysphagia in a patient with a history of GERD Dysphagia to solids that is only gradually progressive is suggestive of an esophageal stricture. GERD accounts for approximately 70-80% of all cases of esophageal stricture. Esophageal web: thin membranes in the mid-upper esophagus. May be congenital or acquired Plummer-Vinson: esophageal webs + dysphagia + iron deficiency anemia A Schatzki ring is a diaphragm-like mucosal ring that forms at the esophagogastric junction (the B ring). If the lumen of this ring becomes too small, symptoms occur Diagnosed by upper endoscopy to determine the underlying cause, exclude malignancy, and perform therapy (dilation) if needed Barium contrast esophagram (barium swallow) can be used as the initial test (prior to upper endoscopy) in patients with clinical features of proximal esophageal lesion or known complex (tortuous) stricture Treat with endoscopic dilation

Hemorrhoids

Patient with internal hemorrhoids will present as → a 43-year-old who has recently noticed bright red blood on the toilet paper when he wipes. He denies any fatigue, decreased exercise tolerance, abdominal pain, or maroon-colored or black, tarry stools. He has no family history of colon cancer. He has never had a colonoscopy. On physical exam, his temperature is 98.6 F, heart rate 70/min, and blood pressure 120/75 mmHg. He does not have conjunctival pallor. There are no abnormalities on cardiac, pulmonary, and abdominal exams. Varicose veins of anus and rectum Risk factor: Constipation/straining, pregnancy, portal HTN, obesity, prolonged sitting or standing, anal intercourse Hematochezia - rectal bleeding (BRPPR), painless, fecal soilage DX: Anoscopy if BRBPR or suspected thrombosis External - lower 1/3 of the anus (below dentate line) Thrombosed:Significant pain, and pruritus but no bleedingPalpable perianal mass with a purplish hueTreat with excision for thrombosed external hemorrhoids Internal - upper 1/3 of the anus Bright red blood per rectum, pruritus and rectal discomfort Treatment: Fiber, sitz bath, ice packs, bed rest, stool softeners, topical steroidsRubber band ligation If protrudes with defecation, enlargement, or intermittent bleedingClosed hemorrhoidectomy if permanently prolapsed

Peripheral vascular disease

Peripheral artery disease is atherosclerotic disease of the lower extremities (and vessels outside the heart and brain) Sx: intermittent claudication = MC presentation; reproducible pain/discomfort in lower extremity brought on by exercise with exercise and relieved with rest; erectile dysfunctionAortic bifurcation common iliac = buttock, hip ground claudication Leriche syndrome refers to a buildup of plaque in the iliac arteries → claudication, impotence, decreased femoral pulsesFemoral artery: thigh/upper calf claudication (MC)Popliteal artery: lower calf claudication Signs: weak or absent distal pulses, arterial bruits, loss of hair, shiny atrophic skin, pallor with dependent rubor The 6 P's caused by acute arterial embolism: pain, pulselessness, pallor, paresthesias, poikilothermia (inability to regulate temperature), paralysis DX: arteriography is the gold standard (clinically only done if revascularization is planned); Doppler ultrasonography; ankle-brachial-index (ABI) < 0.9 (normal = 1-1.2) A falsely high index may indicate severely hardened, non-compressible leg vessels TXt: Risk factor modification: discontinue tobacco, control diabetes, hypertension, hyperlipidemia Medications: B-blocker, ACE-I, statinsPlatelet inhibitors:cilostazol = mainstay of treatment (helpful for intermittent claudication)aspirinclopidogrel (Plavix) Revascularization: Angioplasty → Fem-pop bypass → Endarterectomy TX: aspirin, cilostazol, rosuvastatin, smoking cessation, structured exercise

Ventricular arrhythmias

Premature ventricular contractions (PVCs): Early wide "bizarre" QRS, no p wave seen Ventricular tachycardia: Three or more consecutive VPBs, displaying a broad QRS complex tachyarrhythmia Ventricular fibrillation: Erratic rhythm with no discernable waves (P, QRS, or T waves) Torsades de pointes: Polymorphic ventricular tachycardia that appears to be twisting around a baseline

Hypertension

Primary hypertension is defined as a resting systolic BP ≥ 130 or diastolic BP ≥ 80 on at least two readings on at least two separate visits with no identifiable cause ACC/AHA classification of BP Normal: < 120/80 mmHg and < 80 mmHg Elevated: 120-129 mmHg and < 80 mmHg Stage 1: 130-139 mmHg or 80-89 mm Hg Stage 2: ≥ 140 mm Hg or ≥ 90 mm Hg JNC 8 hypertension definitions not addressed but treatment threshold defined (see below) For children between 1 and 13 years of age: Normal BP: Both systolic BP (SBP) and diastolic BP (DBP) <90th percentile Elevated BP: SBP and/or DBP ≥90th percentile but <95th percentile, or 120/80 mmHg to <95th percentile (whichever is lower) Stage 1 hypertension: SBP and/or DBP ≥95th percentile to <95th percentile + 12 mmHg, or 130/80 to 139/89 mmHg (whichever is lower) Stage 2 hypertension: SBP and/or DBP ≥95th percentile + 12 mmHg, or ≥ 140/90 mmHg (whichever is lower) ACC/AHA blood pressure targets Target blood pressure: < 130/80 Targets for patients with comorbidities: < 130/80 JNC 8 treatment targets: Reduce BP to < 140/90 mm Hg for everyone < 60 including those with a kidney disorder or diabetes Reduce BP to < 150/90 mm Hg for everyone ≥ 60 Treatment guidelines: Normal: evaluate yearly and encourage healthy lifestyle changes Elevated: Recommend healthy lifestyle changes and reassess in 3-6 months Stage 1: Assess ten-year risk using the ASCVD risk calculatorIf risk < 10% start healthy lifestyle management and reassess in 3-6 monthsIf risk > 10% or CVD, DM, CKD - lifestyle mod + 1 medication - reassess in 1 monthIf goal met after 1 month - reassess in 3-6 monthsIf goal not met after 1 month, consider different med or titrateContinue monthly follow-up until goal achieved Stage 2: Health lifestyle + 2 BP-lowering medicationsIf goal met after 1 month - reassess in 3-6 monthsIf goal not met after 1 month, consider different med or titrateContinue monthly follow-up until goal achieved For NON-BLACK patients, including those with diabetes: Initial treatment should be with either: ACE inhibitor or ARB Long-acting calcium channel blockers (most often a dihydropyridine such as amlodipine) or a thiazide-like diuretic (chlorthalidone or indapamide) For stage 2 HTN: the recommendation is:2 BP-lowering medications of different classes For BLACK adults 2 or more medications are recommended to achieve a target of less than 130/80 mm HgThiazide-type diuretics and/or calcium channel blockers are more effective in black adults at lowering BP alone or in multidrug regimens Some antihypertensives are contraindicated or indicated in certain disorders CCB's for angina pectoris ACEI or ARB for diabetes with proteinuria Ace inhibitors are associated with cough, angioedema and can cause hyperkalemia. They are contraindicated in pregnancy Spironolactone can cause hyperkalemia βblockes contraindicated in Asthma and may cause impotence CCB cause leg edema Verapamil and diltiazem are rate control CCBs α-blockers treat HTN and BPH Hydralazine may cause lupus-like syndrome and can cause pericarditis

Rheumatic heart disease

Rheumatic heart disease is a consequence of rheumatic fever characterized by inflammation and scarring of the heart valves Most commonly affects the mitral valve > aortic valve > tricuspid valve Etiology → at least 1 episode of acute rheumatic fever from group A streptococciCumulative inflammation and scarring of the heart valves resulting from an abnormal immune response to group A streptococciMolecular mimicry between streptococcal M protein and cardiac proteinsCross-reaction of antibodies to streptococcal M protein with self-antigensImmune-mediated (type II) hypersensitivity The disease is characterized by valve regurgitation (early stage), most commonly of the mitral valve and valve stenosis (late-stage)The early-stage may last for years and may be asymptomaticThe onset of symptoms usually occurs 10-20 years after acute rheumatic fever SX: palpitations, dyspnea, mitral regurgitation, mitral stenosis, aortic regurgitation, or aortic stenosis DX: Making the diagnosis: based on clinical presentation and confirmed with echocardiography Echocardiography → valvular abnormalities, including regurgitation or stenosis Labs: ↑ anti-streptolysin O (ASO) titers Histology: Aschoff bodies (granulomas with giant cells) on heart valves TX: Prophylaxis to prevent recurrence or worsening of rheumatic heart diseaseAll patients with rheumatic heart disease should undergo prophylaxis with penicillin for the specified time period belowNo evidence of carditis ⇒ 5 years or until age 21 (whichever is longer)Evidence of carditis without valvular abnormalities ⇒ 10 years or until age 21 (whichever is longer)Evidence of carditis and valvular abnormalities ⇒ 10 years or until age 40 (whichever is longer) Medicalpenicillins for all patients in need of prophylaxissulfadiazine for all patients in need of prophylaxis if patients are allergic to penicillin Operativevalve repair or replacement depending on type and severity of valve pathologySurgical repairPercutaneous intervention

Myocardial infarction

STEMI: myocardial necrosis with acute STE or q waves; coronary artery completely blocked; full thickness of myocardial wall involved; elevated troponin I, troponin T, CK, CK-MB (serial troponins - 3 in 24 hours) Location:Anterior wall - STE in leads I, AVL, V2-V6Inferior wall: II, III, AFVLateral wall: lateral leads - I, AVL, V4-6 and reciprocal STD in inferior leadsPosterior wall: ST depression in V1-3 Tx: beta-blocker + NTG + aspirin and Plavix + heparin + statins + reperfusionDoor to balloon time = 90 minutes!!!; thrombolytic therapy in first 3 hours if PCI not availableCI fibrinolytic: intracranial hemorrhage, ischemic stroke 3 months, suspected dissection, active bleeding NSTEMI: myocardial necrosis but coronary artery not completely blocked - rise in cardiac markers without STE or q wave Labs: Troponin at 2-4 hours, peaks 12-24 hours, lasts 7-10 days CK/CK-MB: appears at 4-6 hours, peaks 12-24, returns normal 48-72 hours Myoglobin: appears at 1-4 hours, peak is 12 hours, returns to baseline within 24 hours Tx: beta-blocker + NTG + aspirin and Plavix + heparin + ACE-I + stain + reperfusion (less time-sensitive than STEMI

Angina

Stable angina: Predictable, relieved by rest and/or nitroglycerine Stress test demonstrates reversible wall motion abnormalities/ ST depression >1 mm Angiography provides a definitive diagnosis Treatment: Beta-blockers and nitroglycerin Severe: angioplasty and bypass Unstable angina: Previously stable and predictable symptoms of angina that are more frequent, increasing or present at rest Chronic angina—increasing in frequency, duration, or intensity of pain New-onset angina—severe and worsening Angina at rest Treatment Admit to the unit with continuous cardiac monitoring, establish IV access, O2 Pain control with NTG and morphine ASA, clopidogrel, Beta-blockers (first line), LMWH Replace electrolytes If the patient responds to medical therapy → stress test to determine if catheterization/revascularization necessary Reduce risk factors: stop smoking, weight loss, treat DM/HTN Heparin Prinzmetal variant angina: Coronary artery vasospasms causing transient ST-segment elevations, not associated with clot Look for a history of smoking (#1 risk factor) or cocaine abuse EKG may show inverted U waves, ST-segment or T-wave abnormalities Preservation of exercise capacity Treatment: Stress testing with myocardial perfusion imaging or coronary angiography Pharmacotherapy SL, topical, or IV nitrates (initial) Antiplatelet, thrombolytics, statins, BB Once diagnosis made—CCB and long-acting nitrates used for long-term prophylaxis (amlodipine)

Varicose Veins

Sx: asymptomatic; aching and fatigue Signs: dilated, tortuous veins; greater saphenous = MC; flat, reticular veins; telangiectasia; spider veins Diagnostics: duplex ultrasonography Management: weight loss, control risk factors; graduated compression stockings Interventions: exercise programs, elevation, radiofrequency or laser ablation, compression, sclerotherapy, surgical stripping

Phlebitis

Sx: superficial = dull pain, erythema; deep = swelling, heat, redness Signs: superficial = erythema, tenderness, induration; deep = heat, edema, Homan's sign (calf pain w foot dorsiflexion) Diagnostics: duplex ultrasonography, venography, D-dimer Management: superficial: bed rest, local heat, elevation, NSAIDs; deep = anticoagulation (prevention is key!!) Interventions: surgery

Chronic Venous Insufficiency

Symptoms: progressive edema, itching, dull pain, ulcerations Signs: shiny, thin, atrophic skin Severe disease: ulceration (stasis ulcer, dermatitis) - PAINLESS Diagnostics: clinical; duplex ultrasonography Management: prevention, elevation, avoid extended standing or sitting, compression hose Interventions: wet compresses, compression boots or stockings, skin grafting

Endocarditis

atient will present as → a 45-year-old female with a long history of a heart murmur with one week of increasing fatigue and low-grade fevers. She had a dental cleaning two weeks ago. She denies any hematuria, neurological symptoms, or changes in the appearance of her hands and fingernails. Her past medical history is otherwise insignificant. On physical exam, her temperature is 38.1 C (100.6 F), heart rate is 92/min, blood pressure is 118/67, and respiratory rate is 16/min. She appears fatigued but in no acute distress. Cardiac auscultation reveals a grade III/VI holosystolic murmur heard best at the cardiac apex in the left lateral decubitus position. Pulmonary, abdominal, and extremity exams are within normal limits. An echocardiogram is performed and is shown here. The patient is admitted and started on empiric IV antibiotics. Three days later, 4/4 blood cultures grow Streptococcus viridans that is highly sensitive to penicillin. Inflammation of the lining or valves of the heart caused by the presence of bacteria in the bloodstream, typically introduced via dental or medical procedures in the mouth, intestinal tract or urinary tract Fever and a new-onset heart murmur Acute bacterial endocarditis: Infection of normal valves with a virulent organism (S. aureus) Subacute bacterial endocarditis: Indolent infection of abnormal valves with less virulent organisms (S. viridans) Endocarditis with intravenous drug users - Staphylococcus aureus Endocarditis with prosthetic valve - Staphylococcus epidermidis Duke's Criteria: Definite: 2 major criteria, or 1 major and 3 minor criteria, or 5 minor criteria Possible: 1 major and 1 minor criterion, or 3 minor criteria Major: Blood cultures: S. aureus, S. viridans, S. bovis or other typical species x 2, 12 hours apartDrug users: Staphylococcus. Non-drug users: Streptococcus Echocardiogram: vegetations are seen (tricuspid-IV drug users, mitral-non drug users) New regurgitant murmur Minor: Risk factor, fever 100.5, vascular phenomena (splinter hemorrhages, Janeway lesions: painless, palms and soles), immunologic phenomena (Osler node: raised painful tender; Roth spots: exudative lesions on the retina) Classic signs of infective endocarditis Osler's nodes - tender "ouchy" nodules Janeway lesions - painless macules Roth spots on the retina Splinter hemorrhages on the nail bed Clubbing Treatment: Empiric treatment: IV vancomycin or ampicillin/sulbactam PLUS aminoglycoside Prosthetic valve: Add rifampin High-Risk patients prophylaxis for procedures: Amoxicillin - 2 g 30-60 minutes before the procedure

Mitral Regurgitation

blowing holosystolic murmur at the apex with split S2 radiating to the left axilla Mitral valve doesn't close fully in systole → blood regurge from LV to LA → murmur Caused by: CAD, HTN, MVP, rheumatic, heart valve infection; apical S3 = volume overload on the ventricle

Mitral Stenosis

diastolic low pitched decrescendo rumbling with an opening snap heart best at the apex with pt. lying lateral decubitus position Leaflets of the mitral valve thicken, stiffen from rheumatic fever → valve doesn't open well in diastolic; cause = rheumatic heart Left atrial hypertrophy, may also have mitral regurge

Aortic Stenosis

harsh systolic ejection crescendo-decrescendo at the right upper sternal border with radiation to neck and apex Dyspnea, angina, syncope with exertion; squatting increases intensity; split S2 Increased BNP, helmet cells (schistocytes); cardiomegaly

Pulmonary Stenosis

harsh, loud, medium pitched systolic murmur heard best at 2nd/3rd left intercostal space that may increase with inspiration Stenosis of pulmonic valve impairs flow across the valve; increases afterload on the ventricle widely split S2; early pulmonic ejection sound; RVH

Pulmonary Regurgitation

high pitched early diastolic decrescendo murmur at LUSB that increases with inspiration Blood leaks abnormally backward from pulmonary artery though pulmonic valve → RV (RHF)

Tricuspid Regurgitation

high pitched holosystolic murmur at LLSB radiates to the sternum and increases with inspiration Tricuspid fails to close fully in systole, blood regurgitates from RV → RA = murmur

Hypertrophic Obstructive (HOCM)

hypertrophic portion of septum; LV outflow tract narrowed - worse with Diastolic heart failure young athlete with positive family history sudden death of syncopal episode; inherited; SCREEN FAMILY PE: sustained PMI, bifid pulse, S4 gallop; high pitched mid-systolic murmur at LLSB increased with Valsalva and standing (less blood in the chamber); decreased with squatting Tx: refrain from physical activity; BB or CCB; surgical or alcohol ablation of hypertrophied septum and defibrillator insertion

Tricuspid Stenosis

mid-diastolic rumbling murmur at LLSB with opening snap RARE! Leaflets of tricuspid valve = stiff/immobile → impaired RV filling from decreased tricuspid valve orifice = increased RA pressure → right and left heart failure

Mitral Valve Prolapse

midsystolic ejection click heard best at the apex Abnormal systolic ballooning in part of the mitral valve into the left atrium

Paroxysmal supraventricular tachycardia

narrow, complex tachycardia, no discernible P waves

Restrictive Cardiomyopathy

right heart failure; a history of infiltrative process; diastolic heart failure; stiff heart muscle Amyloidosis, sarcoidosis, hemochromatosis, scleroderma, fibrosis, cancer PE: pulmonary HTN; normal EF, normal heart size, large atria, normal LV wall, early diastolic filling Tx: non-specific; diuretics, ACE-I, CCB

Aortic Regurgitation

soft high pitched, blowing, crescendo-decrescendo along left sternal border; loud leaning forward/squatting Leaflets of aorta don't close during diastole → blood regurgitates from the aorta into left ventricle → volume overload left ventricle S3 or S4 with severe; water-hammer pulse (arterial pulse large and bounding)