Pulmonary System Study Guide

PULMONARY SYSTE Name Pulmonary Emboli Cause Hx of A fib, estrogen therapy, smoking, surgery, cancer, pregnancy, long bone fractures and prolonged inactivity Impending Respiratory Failure - Asthmatic Exacerbation COPD – can include chronic bronchitis and emphysema CommunityAcquired Pneumonia (CAP) Atypical Pneumonia Signs/Symptoms Strep pneumoniae; H. influenzae; Mycoplasma; Chlamydophila pneumonia; Cystic fibrosis: Pseudomas aeruginosa (Gm-) Mycoplasma; Chlamydophila pneumonia; Legionella Treatments Cyanosis and quiet lungs. May speak in 1-2-word sen tences Epi stat. 911 oxygen, albuterol nebs, parenteral steroids, antihista mines and H2 blocker Concerns Sudden onset dyspnea and coughing. Cough may be productive of pink-tinged frothy sputum. Tachycardia, pallor and feelings of impending doom Tachypnea, tachycardia or bradycardia, cyanosis and anxiety. Patient appears exhausted, fatigued, diaphoretic and uses accessory muscles to help withbreathing. Alveolar damage from loss of elastic recoil of lungs, exposure of irritants Airflow limitation Diagnostics Chronic cough (2 years), chronic sputu m production, shortness of breath worse with physical exertion, progressive symptoms, barrel chest, weight loss; hyperresonance upon percussion, tactile fremitu s and egophony is decreased; CXR may show hyperinflation; bullae sometimes present; coarse crackles Alpha-1 antitrypsin deficiency screening < 45yrs ** pack year smoker – COPD** Sudden onset high fever w/ chills, productive cough and purulent sputum (rust-colored if strep pneumo). c/o pleuritic chest pain w/ coughing and dyspnea Rhonchi, crackles or wheezing with dullness over affected lobe, ± tactile fremitus and egophony; abnormal whispered pectoriloquy Spirometry FEV1/FVC <0.70 postbronchodilation. Classification of severity determined by FEV1 CXR only when trying to R/O pneumonia Chest x-ray-lobar consolidation (note: middle lobe is anterior chest by nipple) CBC: leukocytosis (>10.5) look for anemia Smoking cessation, pneu monia & flu vaccine, Acute exacerbation: SABA, LABA, ICS Acute prednisone 40mg/day x 5-1 0 days **± dyspnea, ± sputum volume & purulence may need antibiotic; higher risk for Strep pneumonia & H. influenzae –Augmentin (avoid due to GI upset) Cefdinir, macrolide (avoid due to CV risk); resp. fluoroquinolone (± tendon rupture) S. pneumoniae: macrolides, doxycycline, DRSP: high dose amoxicillin, resp. fluoroquinolones. Minimum 5 days (most 5-7 days) No comorbidities: Macrolides, doxycycline Comorbidities: resp. fluoroquinolones, or macrolide plus beta-lactam High risk : > 2 exacerbations in last year, FEV1 < 50 %, hospitalized for COP D in past year **rarely see under age 40 Chronic bronchitis: cough with excessive mucous for 3+ months for 2+ years Complex patients with co-morbidities: Multiple meds, drugdrug interactions, drugdisease interactions Flu vaccine > 50yo Pneumo vaccine >65yo Smokers – H. Influenza S. pneumoniae affects young and old Lung cancer can present as recurrent pneumonia Fatigue w/ paroxysmal coughing that’s nonproductive; gradual onset starting like a cold; most continue to work/school regardless of symptoms Wheezing with diffuse crackles/rhonchi, rhinorrhea, erythematous throat Physical, chest x-ray shows diffuse infiltrates, CBC Macrolides, resp. fluoroquinolones, doxycycline; antitussives, fluids/rest ***Legionella – contaminated by inhaling mist from a water source. Also accompanied by GI Symptomatic: dextromethorphan, Tessalon PERLES, guaifenesin, severe wheezing Atrovent or albuterol inhaler consider steroids 40mg for 3-5 days Exacerbation of asthma Pneumonia from secondary infection ***On rare occasion macrolide or doxycycline Acute bronchitis Virus causing inflammation of Upper respiratory tract Sudden onset new cough that’s dry and possible small amts sputum; frequent paroxysms of coughing, possible low-grade fever, wheezing and chest pain w/ cough; cough keeping him awake at night History, possible chest x-ray Pertussis 11yo Complications: Sinusitis, OM, pneumonia, fainting, rib fractures PULMONARY SYSTE Name Tuberculosis Asthma Cause Signs/Symptoms Diagnostics Mycobacterium tuberculosis Fever, anorexia, fatigue, night sweats, cough. As progresses, productive cough w/ hemoptysis and unexplained weight loss Chronic inflammation of bronchial tree Reversible disease Recurrent cough, wheeze (end expiration), shortness of breath and/or tightness of chest due to variable airflow obstruction and bronchial hyperresponsiveness triggered by underlying airway inflammation (predictable pattern of symptoms) Symptoms worse at night or with exercise, viral infections or exposure to smoke Typical early in life onset Triad: wheeze, cough and chest tightness/SOB LUNG CANCER SCREENING ➢ Symptoms: o Chest discomfort, dyspnea, hemoptysis, cough ➢ High risk patients o Age 55-74 who smoked at least 30 pack year and/or have quit in last 15 yrs. o High risk smokers at age 50 ➢ Current limitations include: o High false-positive rate o Radiation exposure from multiple CT scans o Patient anxiety Man tou x test: >10mm QuantiFE RON or T-SPO T IG RA (avail w/in 24h) Sputum – early morning and collect for 3 days – NAAT, C&S and AFB CXR: affects upper lobes ± FE V1 > 12% using spirometry; Height, age, gender PFT measures effectiveness of treatment and exacerbations Asthma X X NEVER!! X X Treatments Report to health department Mantoux positive if induration>5mm: HIV+, recent contact, CXR w/ previous TB disease, Immunocompromised >10mm: immigrants, child less than 4, IV drug users, health care workers, homeless; employees of jails, nursing homes >15mm: person w/o risk Isoniazid (INH) 300mg daily, rifampin, ethambutol and pyrazinamide 3x a week (check baseline liver functions) Rescue meds: SABA long-term control: inhaled corticosteroids Step-up therapy if not controlled; Acute prednison e 40-60 mg/day x 3-10 days Written Asth ma action plan; PEAK flow is used to monitor Well controlled – F/U 3-6 months Not well controlled 2-6 weeks **See all asthmatics in Sept to get on controlled drugs and immunizations COPD Consider steroid first for treatment Anticholinergics are not usually helpful Disease is progressive LABA alone is safe Steroid alone is safe Needs rescue inhaler X X X Concerns Risk factors: HIV, migrants, homeless, inmates and nursing homes Prior BCG vaccine may cause false positive Ethambutol causes optic neuritis – avoid if abnormal vision Consider bone density for those on long-term steroids Treatment Goals: Perform normal activities Minimal to no exacerbations Minimal use of rescue inhaler (<2 days a week) Avoid ED Maintain normal PFT WHEN TO USE INSULIN All Type 1 DM patients Basal insulin with adjustments for meals - Basal 40-50% total daily insulin - Bolus 50-60% total daily insulin, given in response to carb intake post meals and with snacks (2 Units to 15 carbs Type 2 DM patients - At time of diagnosis to achieve initial glycemic control if A1c >9% o Short course 2-3 weeks - A1c > 10% - When > 2 standard agents are inadequate - Start 0.1-0.2 u/kg or 10 units - Adjust 2-4 u (or 10-15%) 1-2x weekly to reach FBG goal (80-130 in am) - If hypoglycemia – decrease by 4 units (10-20%) - If am is reached, but during the day it spikes – o Basal Plus: short acting insulin before biggest meal of day o Basal Bolus: bolus at each meal ENDOCRINE SYSTEM ➢ ➢ ➢ ➢ ➢ Onset 15 min Peak 30 min – 2.5 hr. Duration 4.5 hrs. Short acting (Regular) Intermediate NPH Basal (Lantus Levemir) 30 min 1-5 hrs. 6-14 hrs. None 6-8 hrs. Mixture 70/30 30 min. Rapid acting (Lispro, Aspart) 1 hr. 1 hr. 4.4 hrs. 18-24 hrs. 24 hrs. Levemir usually BID 24 hrs. ➢ ➢ ➢ DIABETIC MEDICATIONS FOR DM Consider what therapeutic goal is? Correction of fasting glucose, postprandial glucose, action on insulin resistance, increasing insulin availability, offloading of glucose? Hypoglycemia risk? Cost? Adverse effects? BIGUANIDE – insulin sensitizer, ³ hepatic glucose production and intestinal glucose absorption. Action on fasting & postprandial. Minimal to NO hypoglycemia when used alone. o Metformin/Glucophage (1500-2000/day prevention) ▪ A1c reduction 1-2% ▪ Contraindicated: eGFR < 45, acidosis, alcoholic, hypoxia, Active liver disease (hep C), heart failure • FYI – can use 1000mg daily for GFR 30-45 – don’t start them on it, but can continue ± B 12 deficiency (after on meds > 5 yrs.) – ok to give in Stage 1 Heart Failure ▪ ▪ Risk of lactic acidosis (rare) ▪ Hold if IV contrast dye testing for 48h ▪ Side effects: diarrhea, flatulence and nausea THIAZOLIDINEDIONE (TZD) – insulin sensitizer. Action on fasting & postprandial. Minimal to NO hypoglycemia used alone. o Pioglitazone (Actos), Rosiglitazone (Avandia) – monitor ALT ▪ A1c reduction 0.7% ▪ Avoid heart disease/CHF, causes edema, rare risk of bladder cancer, liver toxicity, weight gain, fractures SULFONYLUREA – stimulates b-cells to secrete insulin –Action on fasting & postprandial. HYPOGLYCEMIARISK o Glipizide (Glucotrol)**preferred over glyburide in older adult, Glyburide (Diabeta) **long half-life; BEERS criteria avoid, Glimepiride (Amaryl) - cheap ▪ A1c reduction 1-2% ▪ Acts like basal insulin – constant insulin release (less effective after many years) ▪ adjust dose in renal impairment ▪ Side effects: weight gain and hypoglycemia -± insulin release, largely in response to ±blood glucose post meal. Action largely on postprandial. DPP-4 INHIBITOR Minimal to NO hypoglycemia, expensive o A1c reduction 0.6-1.4% o Sitagliptin (Januvia), Saxagliptin (Onglyza), linagliptin (Tradjenta), alogliptin (Nesina) – weight neutral, oral agents o Pancreatitis risk and unexplained joint aches MEGLITINIDE – minimize postprandial hyperglycemia; Repaglinide (Prandin) and Nateglinide (Starlix) GLP-1 AGONIST±–insulin release, largely in response to ±blood glucose post meal. Action largely on postprandial. Minimal hypoglycemia, expensive. Injection only. o A1c reduction 1-1.5% o Exenatide (Byetta, Bydureon), liraglutide (Victoza), albiglutide (Tanzeum), dulaglutide (Trulicity) o Slows gastric emptying, leading to appetite suppression and possible weight loss o N/V, contraindicated in gastroparesis, rare pancreatitis risk, avoid in severe renal impairment or ESRD SGLT2 INHIBITOR – lower plasma glucose by± amount of glucose excreted in urine. Primarily postprandial effect. HYPOGLYCEMIA RISK when used with insulin and insulin secretagogues (Sulfonylurea, DPP-4 inhibitor, GLP-1 agonist) o A1c reduction 0.7-1% o Canagliflozin (Invokana), dapagliflozin (Farxiga), empagliflozin (Jardiance) – weight loss, lowers BP o ±risk GU infection adjust dose in renal impairment, DKA and urosepsis risk ENDOCRINE SYST ADDITIONAL DIABETES CONSIDERATIONS ➢ A – Aspirin (81-162 mg daily) in most, esp. men > 50 and women > 60 with DM and > 1 additional CVD risk factor such as HTN, smoking, family hx ➢ B – BP controlled > 2 agents including ACEI/ARB and thiazide ➢ C – Cholesterol: statin therapy > 40 or hx ACS. Goal Lipids < 100 Creatinine (renal function): serum creatinine, calculated GFR and urine microalbumin annually ➢ D – Diet: limit trans and saturated fat. Schedule with dietician if needed Dental care: reinforce ➢ E – Exercise: > 150 min/week (walking) + resistance exercise 3x week Eye exam: annually (diabetic retinopathy) o Neovascularization (new growth of fragile arterioles in retina), microaneurysms, cotton wool spots, soft/hard exudates ➢ F – Foot exam: visually every visit & monofilament at minimum annually ➢ G – Goals of care SOMOGYI EFFECT ➢ ➢ ➢ ➢ Severe nocturnal hypoglycemia stimulating glucagon to be released from the liver High FBG by 7:00a, usually due to overtreatment with evening or bedtime insulin – more common in Type 1 Diagnosed by checking glucose at 3am for 1-2 weeks Tx: Snack before bedtime or eliminate/lower bedtime NPH/regular insulin DAWN PHENOMENON ➢ Elevation in FBG daily early in morning from increase in insulin resistance between 4 and 8am caused by spike in GH and glucagon ENDOCRINE FACTS ➢ Endocrine works as negative feedback – low level of active hormone stimulates production. ➢ Hypothalamus stimulates anterior pituitary gland into producing stimulating hormones (FSH, LH, TSH) – these hormones tell organs to produce hormones. ➢ Hypothalamus: coordinates nervous and endocrine system by sending signals, produces neurohormones that stimulate or stop production ➢ Pituitary Gland: Hypothalamus TRH, GnRH, CRH, GHRH, Somatostatin 1 cm in diameter o 5% chance of malignancy ➢ Malignant Thyroid Nodule o Hx head or neck irradiation o Size > 4 cm o Firmness, Nontender on palpation o Relatively fixed position (non-mobile) o Persistent Nontender cervical lymphadenopathy o Dysphonia o Hemoptysis ➢ TSH, Thyroid ultrasound o ±TSH – metabolically inactive (most common) ▪ Fine needle aspiration biopsy (refer) • Most cost effective o ³ TSH – metabolically active ▪ Nuclear med thyroid scan • Hot – metabolically active o radioactive ablation or surgery • Not hot – metabolically inactive o Fine needle aspiration o Cold usually cyst HYPERTHYROID Smooth, silky Hyperreflexia 6.5% Fasting blood glucose >126 Random glucose >200 with polydipsia, polyphagia, polyuria and unexplain ed weight loss OGTT > 200 Insulin resistance with eventual insulin deficiency Diabetes Mellitus Type 2 Risk factors: age > 45 overweight or obese, abdominal obesity, sedentary lifestyle, family hx 1st degree relative, HTN, HLD < 35, PCOS, hx vascular disease, metabolic syndrome, Hispanic, African American, Asian or American Indian • • Few if any symptoms, usually dx during routine screening; acanthosis nigricans (cutaneous manifestation of hyperinsulinemia) commonly seen on groin folds, over knuckles and elbows – will regress with weight loss and physical activity Screening ADA: Annual for BMI > 25 and 1+ risk factor Everyone > 45 every 3 years if normal A1c > 6.5% IFG > 126 Random glucose >200 with polydipsia, polyphagia, polyuria and unexplain ed weight loss OGTT > 200 Treatments Check A1c q3month s until well-controlled Lipid profile yearly Yearly urine for microalbuminuria ACEI or ARB for HTN (helps renal system) Every visit : BP, feet, lifestyle - healthy eating, weight control, ± physical activity (150 min. week); <140/90 (ADA prefers <130/80) Yearly: flu shots, Aspirin 81mg daily, yearly eye exa m/dental exam, thyroid, lipid profile, urine microalbuminuria Set A1c goal with patient. A1c goal: <7% for most, 6% with low risk, <8% for elderly (varies with pt. attitude, risk for hypoglyce mia, life expectancy, shorter duration with tighter control, comorbidities) Pre-prandial 80-130; Peak postprandial < 180; Bedtime 90-150 Start with Metformin (always prescribe with largest meal of day 500mg ² 1000 mg ² 1500mg ² 20 00 mg) Need ACEI multi drug combo such as: patient specificmetformin, sulfonylurea (improve fasting) add DPP4 (post meal insulin release) Concerns Microvascular: retinopathy, nephropathy and neuropathy Macrovascular: atherosclerosis, CAD, MI Increased risk (diabetic in training) A1C 5.7-6.4% IFG 100-125 IGT= 140-199 ***A1c2 X year in those meetin g goals and quarterly in those not meetin g goals Meds that can ± risk of Type 2 DM – glucocorticoids, HCTZ, atypical antipsychotics, statins Dual Therapy: Metformin Plus Sulfonylurea TZD DPP4 Efficacy High High Intermediate Hypoglycemia Risk Moderate Low Low Weight Gain Gain Gain Neutral Side Effects Hypoglycemia Edema, CHF, Fracture Rare Cost Low Low High Metformin unless contraindicated A1C > 9: Consider dual therapy initially A1C > 10-12: injectable insulin until less glucose toxic BG > 300: injectable insulin until less glucose toxic ***Meglitinides for irregular eating schedule DC sulfonylureas, glitazone after initiating insulin (SU plus insulin is less efficacious with more weight gain) SGLT2 Intermediate Low Loss GU, dehydration High GLP – 1 High Low Loss GI High GASTROINTESTINAL SYS ➢ ➢ ➢ ➢ CONSTIPATION Idiopathic and functional Lifestyle factors o Immobility o Low-fiber diet o Dehydration o Milk intake o Ignoring the urge to have BM Drugs contributing to constipation o Iron supplements o Beta-blockers o Calcium channel blockers o Antihistamines o Anticholinergics o Antipsychotics o Opiates o Calcium-containing antacids Treatment o Bowel retraining o Dietary changes o Ingest bulk forming fiber (25-35 g/day) o Increase physical activity o Increase fluid intake (8-10 glasses) o Consider laxatives ANAL FISSURE ➢ Ulcer or tear of anus, most often posteriorly ➢ Severe anal pain (razor blades) with bowel movements lasting hours after the BM – pain leads to constipation and drops of blood when wiping ➢ Risk factors include constipation, diarrhea, childbirth, anal sex ➢ Primary treatment is to prevent constipation - ± dietary fiber, laxative (mineral oil – avoid long term use due to inability to absorb A, D, E, K vitamins), sitz bath, cool compresses. If these measures fail NTG, Botox, surgical sphincterotomy HEMORRHOIDS ➢ Grade I – no prolapse, Grade II – prolapse upon defecation but reduce spontaneously, Grade III – hemorrhoids prolapse upon defecation and must be reduced manually, Grade IV – hemorrhoids are prolapsed and cannot be reduced manually. ➢ ± risk excessive alcohol, chronic diarrhea or constipation, obesity, high fat, low fiber diet, prolonged sitting, sedentary lifestyle, anal intercourse and loss of pelvic floor muscle tone. ➢ IgG – produce after the infection is Gone o Antibodies present (immune) ▪ No virus / not infected ➢ IgM – antibody you make the Minute you getinfected o Acute infection – contagious ▪ No immunity ➢ Hepatitis A o Fecal-contaminated food/water o Anti-HAV IgG – positive ▪ Immune to HAV o Anti-HAV IgM –positive ▪ Acute infection o Anti-HAV IgM and IgG negative – no immunity, needsimmunization ➢ Hepatitis B o HBsAg – (surface antigen) screening for Hep B ▪ Positive –has virus on board o Anti-HBs (surface antibody)– positive ▪ Antibodies present / immune o Anti-HBc (totally Hep B core antibody) ***rotten to the core*** o IGM anti-HBc ➢ Hepatitis C o Injection drug use o Anti-HCV – screening for Hep C (? Exposure – if negative order HCVRNA) ▪ If positive – order HCV RNA or PCR to r/o chronic infection • If positive RNA/PCR has Hep. C – refer o Screen those born from 1945-1965 ➢ Hepatitis D o Requires presence of Hep. B. Can be acute/chronic o Infection of B/D increases risk for cirrhosis and liverdamage ➢ GASTROINTESTINAL SYSTEM ➢ Psoas/Iliopsoas (supine) –Flex hip 90° have pt. push against resistance and to straighten leg ➢ Obturator sign (supine) – Internal rotate right hip full ROM. + pain with movement/flexion of the hip ➢ Rosving’s sign – Deep palpation of LLQ = pain RLQ ➢ McBurney’s point – Area between superior iliac crest and umbilicus in RLQ ABDOMINAL MANEUVERS ➢ Markle Test (heel jar) – o Raise heels then drop suddenly or jump. Positive if pain is elicited or pt. refuses due to pain. ➢ Involuntary Guarding o Abd. Muscles reflexively become tense when palpated ➢ Rebound tenderness/Blumberg o Abdominal pain worse when palpating hand releases suddenly ➢ Murphy’s maneuver – Press deeply RUQ under costal border during inspiration. Mid-inspiratory arrest + finding ➢ Cullen’s sign –edema and blue discoloration around umbilicus ➢ Grey Turner’s sign –blue discoloration on flanks that may indicate retroperitoneal hemorrhage RANDOM INFO ➢ Prolonged PPI Usage o Vitamin B12, calcium, magnesium, iron malabsorption, possible ±fx and C. diff risk ➢ Partial obstruction plus chronic low volume bleeding o Esophageal Stricture o Esophagitis o Esophageal Cancer ▪ Needs endoscopy ➢ Bowel obstruction – abdominal pain associated with dilated loop of bowel and tinkling bowel sounds. KUB – ileus. Refer ➢ Ileus – absent bowel sounds – KUB ➢ Gilbert’s Disease - ± Bilirubinonly ➢ Acute abdominal pain LUQ for 60 minutes - EKG LFT’S ➢ Aspartate Aminotransferase – (AST) (SGOT) present in liver, heart, muscle, kidney and lung ➢ Alanine Aminotransferase – (ALT) (SGPT) found mainly in liver; + liver inflammation – more specific for hepatic inflammation o If both AST and ALT elevated ▪ ALT > AST – (liver) think hepatitis ▪ AST > ALT - (Acetaminophen, Statins, Tequila) ➢ AST/ALT Ratio o 2.0+ = alcohol abuse o 1-2 = ETOH, liver disease o <1 = fatty liver disease ➢ Serum GGT – elevated in liver abuse and acute pancreatitis; sensitive for alcohol abuse ➢ Alkaline Phosphatase – (ALP) enzyme derived from bone, liver, gallbladder, kidneys, GI and placenta. ±levels seen during growth spurts; healing fractures, osteomalacia, bone malignancy, vitamin d deficiency, Paget’s, bone cancer o Expect elevation in pregnancy and kids ➢ Albumin – liver makes albumin ➢ GASTROINTESTINAL SYSTEM Name Cause Signs/Symptoms Acute onset periu mbilical pain steadily worsening over 12-24 H . Pain localizes at McBurney ’s point with rebound and guarding, anorexia. Psoas and obturator signs + If ruptures, have guarding, rebound, and board like abdomen. Severe RUQ or epigastric pain constant with 23 minutes of increased pain (colicky pain) can occur w/in 1h of consumin g fatty meals. Pain can radiate to right shoulder, N/V, anorexia, intermittent fever, + Murphy’s sign Diagnostics CT with contrast **Abd US can be used in younger thinner people Left shift: ± WBC, ± neutrophils, ± Bands REFER Elevated AST, ALT and ALP RUQ abdominal US - HIDA Gut rest with clear liquids REFER to Surgery Acute Appendicitis Inflammatory disease caused by infection or obstruction Acute Cholecystitis Inflammation of gallbladder nearly always caused by gallstones Acute Diverticulitis Infected diverticula (diverticulosis most common in sigmoid colon) Fever, anorexia, nausea, cramping, LLQ pain. - Blumberg’s sign; Acute abdomen rebound, Rovsing +, board like abdomen. Diverticulosis – exam normal 33% of population will develop diverticulosis by age 50 CBC shows leukocytosis w/ neutrophilia Bands signal severe bacterial infection; FOBT + if bleeding CT scan definitive scan Drug use, Alcohol abuse, gallstones, elevated triglycerides, infections Acute onset fever, N/V associated with rapid onset severe abdominal pain radiating to mid-back with bloating. Guarding and tenderness over epigastric region on exam. + Cullen’s sign and Grey-Turner’s sign **rocks back and forth to relieve pain ± serum amylase, lipase and trypsin; ± AST and ALT, GGT, bilirubin, leukocytosis; abdominal ultrasound and CT Triglycerides > 800 ± risk Acute Pancreatitis Severe watery diarrhea 10-15 stools a day w/ lower abdominal pain, cramping and fever. Symptoms appear 5-10d after antibiotic initiation (clindamycin, quinolones, cephalosporins and PCNs) Clostridium difficile Colitis (C-diff) Colon Cancer adenocarcinomas 3rd leading cause of cancer deaths in US Crohn’s Disease Inflammatory bowel disease affecting mouth to anus (Inflammation affects entire intestine wall) Ulcerative Colitis Inflammatory disease affecting colon/rectum (Inflammation affects mucosa) Asymptomatic until advanced disease. Vague GI symptoms, changes in bowel habits, stool or bloody stool. Heme-positive stool, dark tarry stool, mass on abdominal palpation. May have hx of polyps fever, malaise and mild weight loss, periumbilical to RLQ pain. May palpate tender abdominal mass. Remission and relapses are common. If ileum involved, diarrhea without blood or mucous. If colon involved bloody diarrhea with mucus. Fistula formation and anal disease. bloody diarrhea with mucus. Severe 15,000) Stool assay for C-diff Metronidazole (Flagyl), avoid antimotility agents and opiates, increase fluid intake Colonoscopy age 50 (repeat every 10 yrs. unless polyps) <40 assess cancer risk; FOBT annually ever year; Cologuard every 3 yrs. Screen everyone with these questions: Have you ever had colorectal cancer (CRC) or adenomatous polyp (AP)? Inflammatory bowel disease? Family member with CRC or AP? If CRC - Surgery, chemo and radiation ± risk factors >50 yrs.; multiple polyps or inflammatory bowel disease (diet in high fat, red meat and low calcium may contribute Lactulose intolerance is common. Stop smoking. Gut rest. Oral aminosalicylates sulfasalazine and mesalamine (better tolerated). Flagyl and Cipro. Immune modulators ±risk of toxic megacolon and colon cancer; risk of development of lymphoma especially when treated with azathioprine. More common in Jews Oral aminosalicylates sulfasalazine and mesalamine (better tolerated) Corticosteroids. No antibiotics due to risk of C. Diff. Immune modulators ± risk of toxic megacolon and colon cancer ± CRP, ESR, Leukocytosis Anemia (chronic disease, B12 deficiency) WBCs in stool Cobblestone mucosal pattern on endoscopy – skin lesions ± CRP, ESR, Leukocytosis Anemia WBCs in stool