533-Exam-2-Comp-Notes

○ R/O life threatening events → 911!!!!! ■ Aortic dissection ● Sharp tearing pain into the back ● SEND TO ER IMMEDIATELY!!! ■ MI ■ Pulmonary embolism ■ Spontaneous Pneumothorax ● Exercise Stress test results ○ Ischemia = horizontal or down-sloping of the ST segment, ST depression > 1 mm, 60-80 milliseconds after the J point ○ Negative standard ECG responses ■ No ST segment depression ■ J-point only depression ○ Equivocal standard ECG response ■ Upsloping ST segment depression ○ Positive standard ECG responses ■ Horizontal ST segment depression ■ Downsloping ST segment depression ○ Duke Treadmill score ■ Exercise duration in min - (5 x ST deviation mm) - (4 x Angina index) = Duke ■ Angina index ● 0- non, 1- typical angina, 2- angina causing test cessation ■ Score ● > 5 low risk Indicates a 5 year survival rate of 97% ● -10 to 4 = intermediate 5 year survival of 90% ● < -11 = high 5 year survival of 65% ● Labs ○ Lipid profile ○ HgA1c ○ CBC, Creatinine, BNP ■ Look for anemia ● Pts who have a hgb < 7 can have a ST seg depression or T wave inversion ■ Polycythemia, thrombocytosis - elevated plts ● Anything that increases the viscosity of the blood can impede coronary artery blood flow ■ BNP checks for evidence of heart failure ● Management of Stable CAD ○ Goal is to prevent a major coronary event ■ Make sure BP is under control (130/80), DM under control, exercising, not smoking, weight loss ■ Exercise is recommended 30 min 5 to 7 times a week ● Wt loss can have a significant impact on decreasing complications from CAD & actually improve their comorbidities ○ Non-modifiable risk factors ■ Age, gender ■ Genetics, race & ethnicity ○ Modifiable risk factors ■ High BP, smoking ■ DM, physical inactivity, obesity, high blood cholesterol ○ Secondary Prevention ■ Statins ● High intensity vs moderate intensity ○ High if under 75 yo ○ Moderate or high if over 75 yo ● AHA/ACC ■ BP control ● Goal: < 140/90 vs 130/80 ● ACEI/ARB

■ Pain & symptoms usually occur @ rest or w/ min exertion and lasts longer than 20 min ○ 2. Nausea, feeling light-headed or unusually tired ○ 3. Pain or discomfort in the jaw, neck or back ○ 4. Pain or discomfort in the arm or shoulder ○ 5. SOB ● Evaluation ○ VS ○ EKG w/in 10 min!!!! ■ STEMI ⇒ refer onto a PCI capable center w/inn 90 min ● Outcomes are better w/ PCI ■ Look at least to see where infarction or ischemia is ○ Aspirin 162 mg to 325 mg ○ Oxygen if O2 sat < 90% or respiratory distress ○ Nitro if BP can tolerate it for STEMI ○ Physical exam ■ Appears uncomfortable, diaphoretic, pale, cool skin, ashen ○ Refer to ED ■ Troponin T & I ● Peak w/in 3 to 4 hours ● Checked every few hours to see if it’s increasing ● Can remain positive for 7 to 10 days after there is injury ● ■ Chest x ray ● Looks for other etiologies of chest pain ex. PNA or pneumothorax ■ Coronary angiography if uncertain of acute coronary syndrome ■ Echo ● Done to detect any sort of wall motion abnormalities that can occur w/ acute MI ■ EKG changes ● Inferior leads are II, III, aVF ○ If there’s a stemi in leads II and III and then reciprocal leads (ex. lead I) ST segment depression & t wave inversion= STEMI ● New onset Left BBB = STEMI ○ Sometimes we don’t know if it’s new ○ No evidence that they had it before, consider it new ● Uwave ○ Small deflection following the T wave ○ Benign if 5 mm or less & deflect in same direction as T wave ○ Can also indicate an acute MI, non specific ○ Can occur with electrolyte imbalances or cardiomyopathy, hyperthyroidism ● ST depression ≥ to 2 mm in the precordial leads (V1 to V4) may indicate transmural posterior injury; multi lead ST depression with coexistent ST elevation in lead aVR has been described in patients with left main or proximal left anterior descending artery occlusion. ● Evolution of MI ○ Acutely w/in mins pts develop STEMI ○ Hours later develop Q wave ○ 1-2 days later , ST segment resolves ○ Q wave still present, deep & wide = old MI

■ Right sided - usually results from advanced left sided ● Lower extremity edema, fatigue, exercise intolerance, JVD ● Nocturia, ascites, hepatomegaly, decreased appetite, nausea ● S3 heart sound ○ Labs/Tests ■ Chest X-ray ● Look for other causes of dyspnea ● In HF pts - cardiac silhouette is enlarged , cardiomegaly ● Definition of the pulmonary vessels are obscured due to surrounding edema ■ CBC, Electrolytes w/ Ca & Mag ● CBC to look for anemia ■ BUN & creatinine, UA ■ Glucose, fasting lipids, LFTs, TSH ● Hyperthyroidism can exacerbate HF ■ BNP or N-terminal pro-brain natriuretic peptide (NT-proBNP) ● BNP is very sensitive, good at r/o HF ○ Can be used in pts who are stage B HF ● BUT don’t use BNP in pts who take an ARNI ○ Check proBNP instead ○ Dx ■ Echo ● Most valuable tool when assessing HF ○ Calculates EF ● Ventricular ○ Function ○ Thickness ○ Wall motion of myocardial tissue ○ Size ● Valves ○ Look for valvular dz, look for regurgitation or stenosis ■ EKG ● Look for infarction, ischemia, LVH, arrhythmia ■ Dx criteria: *At least 2 major and 2 minor*. Positive likelihood ratio = 10, negative likelihood = 0.4 ● **More helpful for ruling in HF not r/o!** ● If they meet these criteria → refer for ECHO!!! ○ ***Elevated BNP but don’t meet all criteria? Still get an ECHO!!!!** ● Major criteria ○ Acute pulmonary edema ○ Cardiomegaly ○ Hepatojugular reflux ○ Neck vein distention ○ Paroxysmal nocturnal dyspnea/orthopnea ● Minor criteria ○ Ankle edema ○ Dyspnea on exertion ○ Hepatomegaly ○ Nocturnal cough ○ Pleural effusion ○ Tachycardia > 120 HR ● Heart Failure Classification & Management ○ New York Heart Association (NYHA) & American Heart Association American College of Cardiology (AHA/ACC) Classification ■ Helps determine what your tx is going to be for the pt ○ NYHA ■ Classification based of symptom severity & amount of exertion needed to provoke symptoms

● Offer diuretics as needed to relieve symptoms if they have symptoms of congestion ● Treat their comorbidities ex. DM, HTN, CAD ■ Reduced ejection fraction, management is different ● Meds: Beta blocker, ACEI or ARB, diuretics ○ ANRIs if pt intolerant to ACE or ARB ○ **Thiazide diuretics less potent than loops ** ○ Aldosterone antagonists can be used, adding onto beta blockers, block RAAS ● Watch creatinine, renal function ● W/ any start or increase in the dose, monitor potassium closely, especially starting a pt on an aldosterone antagonist ● Meds for specific populations ○ Hydralazine w/ isosorbide dinitrate for AA pts or pts who cannot tolerate ACE/ARB ○ Another add on is ivabradine ■ Added on as an adjunct & considered more for a class II & III HF ○ Digoxin for certain patients ■ NOT II or III, more for severe HF pts ■ Positive inotrope ● ICD for Select pts between stage B or D who have an EF < 35% who are on max med therapy ● Stage D ○ Marked HF symptoms, recurrent hospitalizations ○ Goal→ Control s/s, improve QOL ○ Pts are managed by cardiology ○ Possibly palliative care is involved ○ More advanced care measures managed by cardiology

■ Look at size of heart ■ R/O other pulmonary etiologies ○ Labs ■ CBC w/ diff, Inflammatory markers ● Inflammatory markers often elevated! ■ Troponin ● Elevated in 30-40% of pts w/ acute pericarditis ● Gets better after a week, declines ● Transient elevation ○ ECHO ■ May be normal, may show a pericardial effusion ● Fluid in pericardial sac ■ Mild cases may not show effusion or small effusion ■ Large effusion? HIGH RISK → Hospitalize that ish ● Dx ○ 2 of the following criteria: ■ Sharp pleuritic chest pain ■ Pericardial friction rub ■ EKG changes ■ New or worsening pericardial effusion ○ Inflammatory markers help support the dx ● Management ○ Low risk ■ Stable, no fever, do not have large effusion ■ NSAIDS, start at max dose ● Slowly titrate down over 3-4 wks ■ Return to clinic regularly ■ Monitor inflammatory markers & symptoms ● Watch markers decrease, once back to normal → pericarditis has resolved ■ Not getting better w/in 7 days ? Hospital & cardio referral Approach to Patients w/ Acute Chest Pain ● What to do! ○ 1st determine if it is stable or unstable? ■ Unstable? Bye bye go to the ER please thanks don’t die ○ Consider risk factors ■ Old pt ex. Man > 50 yo, woman > 65 yo w/ CVD or risk factors for CVD who’s coming in w/ chest pain ○ Evaluate them! ■ STAT EKG w/in 10 min of presentation ■ Refer to ED for further eval to r/o ACS ○ Differentials - Always think about cardiac, pulmonary, GI, MSK, skin & psych differentials!! See Table 102.5 in Buttaro pg 568 ■ Aortic dissection, pulmonary embolism, MI, & spontaneous pneumothorax must be considered, expediently detected, dx, & managed in the differential diagnosis of chest pain. ■ Determine if chest pain is pleuritic or non-pleuritic ● Onset, quality, quantity, duration, what helps? What makes it worse? ● Pleuritic chest pain is worse w/ inspiration & expiration ■ Pulmonary Embolism ● Pain anywhere w/in the chest ● May be more localized, may be on one side of the chest, may be felt more in the back ● Risk factors ○ Do you smoke? Did you recently take a long flight or have surgery? ○ Underlying health conditions that would increase risk of PE ● S/S ○ Pleuritic pain, sharp in nature, SOB

● Herpes zoster ○ Get prodrome of pain, can be severe ○ Do a good skin exam looking for vesicular lesions w/ pain that does NOT cross the midline ○ Along the dermatome or nerve pain ■ Psych ● Panic disorders ○ Can manifest w/ chest pain and SOB, acute episode ○ Ask about anxiety!!! ■ I think in this class we all have panic disorders Cardiac Diagnostic Testing Heart Murmurs & Dysrhythmias Review of Cardiopulmonary Circulation ● Blood flow ○ Systemic flow returning to the heart ■ Deoxygenated blood comes back to the heart → vena cava → right atrium → tricuspid valve → right ventricle → pulmonary valve → pulmonary artery → lungs for gas exchange, now the blood is oxygenated yay → pulmonary vein → left atrium → mitral valve → left ventricle → aortic valve → aorta → systemic systems to oxygenate dat bod When to say goodbye to your patients w/ murmurs according to Buttaro: ● Cardiology Referral: ○ Pathologic murmurs or concerning signs that require evaluation by a cardiologist include: ■ Diastolic murmurs, holosystolic murmurs, systolic murmurs grade 3 or above , a murmur with a new extra heart soun d (S3, S4, or a click), or a murmur that increases in intensity when the patient stands. ● Hospitalization: ○ Acute or chronic valvular disease that becomes hemodynamically unstable or requires acute management of complications— such as heart failure, pulmonary edema, or uncontrolled angina — requires hospitalization.

■ Recognize and dx then refer to cardio ○ Referral ■ Cardio does further refinement of dx, specifically what is wrong with the valve and then initiate meds ○ Management ● Referral Guidelines for VHD ○ Recognition and diagnosis by primary care physician (PCP) ○ Referral to general cardiology ○ Level II primary valve center ■ Multidisciplinary teams ■ Surgical replacement w/ or w/o a CABG ○ Level I primary valve center ■ If they require intervention ■ Multidisciplinary teams ■ Transcatheter valve replacement ● Less invasive ● Infectious Endocarditis Prophylaxis ○ Antibx prior to procedures ○ Affordable care act guidelines (ACA) & ACC ■ Recommended for pts that have had a transcatheter prosthetic valve or pts w/ prosthetic material in their valve repair ■ If pt has hx of infectious endocarditis Systolic Heart Murmurs ● Acronym to help you out! Yay football! MR. PM AS MVP ○ Mr. Payton Manning as MVP ● Aortic Stenosis (AS) ○ Most commonly age-related calcification ■ Age 15-65 yo, usually congenital ○ Other causes ■ CAD, chronic trileaflet or deterioration ■ Rheumatic heart dz ← 2nd most common cause

● If rheumatic fever, usually mitral valve involved too ○ Symptoms ■ Occur once valve is stenosed to approx 1 cm squared opening ■ Prolonged asymptomatic period, Can compensate for years until 5-6th decade of life then rapid deterioration @ onset of symptoms ● Often left ventricle hypertrophies ■ Three cardinal symptoms: Exertional dyspnea, angina pectoris, syncope ● 1st symptom usually dizziness ■ HF ● Usually rapid downhill course from here → refer to cardio ■ Fatigue, dyspnea ○ Physical exam ■ Murmur ● Loudest along Right sternal border /2nd intercostal space, carotids or apex ○ Often you can hear it transmitted up into the carotid arteries ● Mid-systolic, low-pitched murmur that is heard best over the base of the heart ● Usually audible S4 , apex impulse is forceful but late as LV dilates ○ Apex becomes diffuse & lateral ● Narrow pulse pressure ■ 1/3rd of pts also have CAD ○ Diagnostic testing ■ EKG ● Usually normal ■ ECHO ● Cardiomegaly appear LATE on echo ■ Consider chest x-ray depending on how symptomatic the pt is ■ Possible referral for cardiac cath ○ Diff dx ■ Aortic stenosis murmur vs hypertrophic obstructive cardiomyopathy ● Have them perform Valsalva maneuver ○ Management ■ If they need more management then meds referred to a valvular center ■ ACEI ■ Manage lipids ● Mitral Regurgitation (MR) ○ Left side of the heart, reflux of blood ■ Blood doesn't all go from left atria to left ventricle, retrogrades back up gross ○ Cause ■ Most commonly rheumatic heart disease ○ Other causes ■ Congenital condition, acute bacterial endocarditis, MVP ○ Course ■ Prolonged asymptomatic period, onset of CHF in 4-6th decade, downhill course over 10 years, eventually LV fails RIP ○ Symptoms ■ Depends on the level of regurgitation & how effectively heart compensates ■ Chronic mild to moderate they often don’t have symptoms ■ As it progresses → fatigue, exertional dyspnea, orthopnea ● Gets worse as it progresses ■ Severe → palpitations, rt sided HF , acute pulmonary edema ■ Symptoms related to bacterial endocarditis ○ Physical exam ■ Systolic murmur ● S1 is absent, mitral listening point

● Holosystolic murmur, more prominent over the apex of the heart, radiates to the axilla & sternum ● Usually Grade 2+ ■ PMI is displaced laterally & is diffuse ○ Diagnostic testing ■ EKG ● Afib is common ■ ECHO ■ Consider chest x ray ● LA & LV enlarged ■ Depending on symptoms → refer for cardiac cath ○ Management ■ Often have comorbid dx of a fib ■ Consider if they need antiarrhythmics or anticoagulants ■ Signs of HF? ● BB, ACEI, diuretics ■ Hx of infectious endocarditis ● Antibx prior to procedures ■ Repair of valve ● Mitral Valve Prolapse (MVP) ○ Most commonly idiopathic ■ A lot of times people don’t even know, asymptomatic ■ Common in women 15-30 yo ■ Can be later onset ■ Redundancy of mitral valve leaflets w/ degeneration of the mitral valve tissue ○ Other causes ■ Marfan syndrome, osteogenesis imperfecta, Ehlers-Danlos syndrome ○ Symptoms ■ May be asymptomatic their whole lives ■ If they experience symptoms it could be palpitations due to SVT or afib, PVCs/PACs, more common w/ exercise, chest pain ■ Dyspnea, dizziness, numbness ○ Physical exam ■ Click ● Mid systolic click & then a high pitched murmur that happens during systole ● Best heard @ apex of the heart & Left sternal border ● Later - late systolic click ○ Accentuated w/ standing ○ Quieter w/ squatting ○ Diagnostic testing ■ EKG ● Usually normal ■ ECHO ○ Management ■ Surgical management if pts experiencing ● pulmonary HTN ● Systolic dysfunction noted in EF ● New onset of afib ● Tricuspid Regurgitation ○ Most commonly functional ■ Reflux in the heart ■ Secondary to marked right ventricle dilation ○ Associated conditions ■ MI w/ right ventricular remodeling that led it to become not as functional ■ Trauma

○ Symptoms ■ Most of the time not symptomatic ■ If they do present w/ symptoms ● Fatigue, exertional dyspnea ■ Severe? Reduced cardiac output ○ Physical exam ■ Prominent right ventricle along the left peristernum ● May feel impulses there ■ Murmur ● Holosystolic murmur in the LLSB ● Increases w/ inspiration, decreases w/ expiration ○ Diagnostic testing ■ EKG ■ ECHO ○ Management ■ Depends on severity ■ May require repair of the valve ■ If rt sided HF ● Tx w/ diuretics, aldosterone antagonists Diastolic Heart Murmurs - ALWAYS bad bad → Cardio referral everytime!!! ● Acronym - ARMS ○ Payton Manning has arms! Crazy! Yay football! ● Aortic Regurgitation (AR) ○ Most commonly rheumatic heart disease ■ Other causes ● Infectious endocarditis, concomitant aortic stenosis, congenital deformity, aortic root abnormalities, syphilis ○ Due to left ventricular dilation → decrease in EF → ischemia due to increased O2 demand ○ Associated w/ angina, HF, dizziness and chest pain ○ Symptoms ■ Usually do not have symptoms for 10-15 years ■ May notice awareness of their heartbeat, palpitations or head pounding ● Palpitations due to tachycardia or premature beats ■ Later have exertional dyspnea, orthopnea, paroxysmal nocturnal dyspnea, diaphoresis, atypical anginal chest pain ● Due to mechanical interaction btw heart & chest wall ○ Physical exam ■ Displaced apical impulse - downward & left ■ Very wide pulse pressures ■ Arterial pulses are wide & quick (water hammer pulses) ■ Murmur ● Mid-systolic ejection murmur → Progresses to low pitched diastolic murmur as it becomes severe ○ Diagnostic testing ■ EKG ● Evidence of LVH - increased R wave amplitude in I, aVL, V4-6 & increased S wave depth in III, aVR & V 1-3 ■ Echo ■ Chest x ray ● LATE finding is very large & dilated left ventricle w/ enlargement downward ■ Possible cardiac cath referral ● Diastolic murmurs typically have a more severe progression ○ Management ■ Acute onset

● Diuretics, vasodilators, ACEI, Ca channel blockers ■ As it progresses, consider valve replacement ● Mitral Stenosis (MS) ○ Most commonly rheumatic heart disease ■ Other causes ○ Course: ■ Stage 1 - Long period asymptomatic → 20 yrs, then gradual reduction in exercise tolerance → 3-5 yrs ■ Stage 2 - Onset of pulmonary Congestion ■ Stage 3 - Development of pulmonary HTN ■ Stage 4 - Severe state of low Cardiac Output ■ **Average age of death = 48 :( ○ Symptoms - depends on the stage ■ Dyspnea, cough, sudden change in heart rhythm & volume status ● Cardiac output is going to be affected ■ Orthopnea, paroxysmal nocturnal dyspnea ■ Pulmonary changes, thrombus, emboli ■ Hemoptysis from increased pulmonary pressures ○ Physical exam ■ Murmur ● Low-pitched, rumbling diastolic radiating toward axilla ● Loud S1 ● Heard best at apex of heart when the pt is lying in the left lateral recumbent position ○ Pushes the heart forward so it’s easier to hear ○ Diagnostic testing ■ EKG ● Afib is common ■ ECHO ● Right ventricular hypertrophy ■ Chest x ray ● Left atrium enlarged ○ Management ■ Often assoc w/ dysrhythmias ● Afib ○ Consider anticoagulants ■ Infectious endocarditis prophylaxis ■ Valve center ● valvotomy to open it up more or do a full on replacement ● Tricuspid Stenosis ○ Most commonly rheumatic heart disease ■ Less common than mitral stenosis but usually due to mitral stenosis ○ Associated conditions ■ Mitral stenosis ○ Symptoms ■ Pulmonary congestion, fatigue ■ Rt sided HF symptoms ● Hepatomegaly, ascites, edema ○ Physical exam ■ Murmur ● LLSB near xiphoid process ● Diastolic ○ Diagnostic testing ■ EKG ■ ECHO ○ Management

■ Think of Rt sided HF management ● Salt restriction, bedrest, diuretics ■ Surgically repaired or replaced depending on severity and what the local area has available Pediatric Heart Murmurs ● Common in asymptomatic healthy children ● May be only exam finding of heart disease ● Collect thorough history ○ Family history ■ Hx of congenital heart dz ○ Perinatal history ■ Poor feeding, failure to thrive ○ Past medical history ■ Any chest pain, palpitations ● Benign or Innocent ○ Result from normal patterns of blood flow ○ Absence of abnormal physical exam, negative ROS ○ Systolic heart murmurs ○ Make up majority of murmurs referred ○ Cannot be determined with 100% accuracy ○ Diagnostic criteria ● Seven Ss of Innocent Murmurs 1. Sensitive a. Does the murmur change w/ the child’s position or respiration 2. Short duration a. Long duration = holosystolic b. Short duration is less concerning 3. Single a. NOT associated w/ a gallop or click 4. Small a. Limited to a small area, non-radiating 5. Soft a. Low amplitude

6. Sweet a. More musical in quality, not harsh sound 7. Systolic a. Diastolic = bad (it ain’t innocent, may have been to prison) ● Red Flags ○ Holosystolic or diastolic murmur ○ Grade 3 or higher murmur ■ Easily heard, moderately lund ○ Harsh quality ○ Abnormal S2 ○ Location at the upper left sternal border ■ Think pulmonary stenosis, pulmonary flow murmurs, atrial septal defects or patent ductus arteriosus ○ Systolic click or gallop ○ Increased intensity with standing ■ Or no change w/ passive leg elevation? Think possibly hypertrophic cardiomyopathy ○ Complaint of chest pain ○ Family history of Marfan syndrome, malformation syndrome, Down ○ Family history of sudden cardiac death ○ Malformation syndrome ○ Increased precordial activity ○ Decreased femoral pulses ○ Abnormal second heart sound ● Indications for Referral ○ For confirmation/clarification of diagnosis ○ If innocent murmur cannot be excluded ○ All children younger than one year of age ■ Due to high rates of asymptomatic heart dz ○ Referral will reduce parental anxiety ● As a PCP your job is to ID that a murmur is present Infective Endocarditis ● Immediate specialist consultation & transfer to the ED is indicated for patients with fever & suspected endocarditis. ● What is it? ○ A microbial infection within the endothelium of the heart. ○ Vegetations form & adhere to the endothelial structures. The heart valves are most often involved, but the disease may also occur w/in a septal defect, on the chordae tendineae, or on the mural endocardium. ● Cause ○ Bacterial most common cause ○ Increasing number of cases caused by fungal, chlamydial & rickettsial organisms ○ In many countries, rheumatic heart disease is still a common cause of IE; it has been implicated in 37% to 76% of infections. ● Acute, Subacute vs Chronic

○ Acute IE is a fulminant process; death can occur within days to less than 6 weeks. ○ Subacute IE (death occurring within 6 weeks - 3 mo) & chronic IE (death occurring later than 3 mo) are usually classified together. ○ Native Valve Endocarditis (NVE) is the most common type of IE & affects the mitral valve (28% to 45%), the aortic valve (5% to 36%), and both mitral and aortic valves (35%); the tricuspid valve is rarely affected (5% to 10%). ● Risk Factors ○ Previous history of endocarditis ○ Valve replacement surgery ○ IV drug use ○ Hospital acquired, usually in pts who underwent surgery ● Presentation ○ Low grade fever, non specific symptoms ○ May present as an acute, rapidly progressive disease ○ Neuro findings ■ Evidence of cerebral emboli ○ Eye findings ■ Roth spots are exudative, edematous hemorrhagic lesions of the retina. ■ Endogenous endophthalmitis can be one of the consequences of IE; usual symptoms are decreased vision and/ or eye pain. It can cause severe vision impairment and vision loss. ○ Cardiac ■ Valvular infection ■ Heart Murmur ● A new murmur of regurgitation or change in an existing murmur suggests an acute, virulent process ■ Development of CHF ○ Pulmonary ■ PE! ■ pleural effusion, pneumonia, pleuritic chest pain, and cough with or without blood-streaked sputum. Pneumothorax may also be a complication of septic pulmonary emboli. ○ Skin ■ Petechiae may be noted on the conjunctiva, palate, buccal mucosa, and extremities; they are present in 20% to 40% of patients and usually only for the first few days. Splinter hemorrhages are linear, subungual hemorrhages appearing in the proximal nail bed, and are common in subacute IE. ■ Janeway lesions and Osler nodes are cutaneous lesions associated with endocarditis. ○ Renal ■ Renal Failure, uremia ○ Musculoskeletal findings ■ Arthralgias and myalgias ■ Myalgias, often localized to the thigh or calf, are commonly unilateral and have no radicular pattern. ● Labs ○ Blood cultures ○ CBC ○ Inflammatory markers ■ ESR elevated ■ Rheumatoid factor elevated if infection lasting 3-6 weeks ○ ECG ○ TTE to ID vegetations ○ TEE preferred for pts w/ valve prostheses ○ Cardiac CT when anatomy cannot be clearly delineated by echo ● Duke Dx Criteria ○ Definite Infective Endocarditis ■ Pathologic criteria ● Microorganisms: documented by culture or histologic examination of vegetation, embolic material, or intracardiac abscess; or

● Pathologic lesions: presence of vegetation or intracardiac abscess, histologic confirmation of active endocarditis ■ Clinical criteria ● Two major criteria; or ● One major criterion and three minor criteria; or ● Five minor criteria Congenital Heart Disease (CHD) ● Hx ○ Fam, Personal ○ Perinatal ■ What happened during the pregnancy ■ Did the mom get prenatal care ■ Any type of substance use that would be concerning/put the child more at risk ○ Down syndrome, other conditions related to CHD ● ROS ○ Cardiovascular, Respiratory ○ Constitutional ■ Fatigue, anorexia, wt loss ● In infant they may be losing weight, failure to thrive, not meeting milestones because they’re in distress while they’re eating due to cardiopulm system not functioning appropriately ● Physical Exam Findings ○ Abnormal growth ○ Abnormal vital signs ■ Tachypneic especially after feeding ○ Adventitious breath sounds ■ One of the major complications of CHD is heart failure ○ Chest contour ○ Dysmorphic features ■ Ex. those found in Down syndrome as they have more incidences of cardiovascular CHD ○ Cardiovascular findings ■ Auscultation points, look at the kid, listen when they’re sitting, standing, lying, left lateral position ○ Gastrointestinal findings ● Hypertrophic Cardiomyopathy ○ Sudden death in athletes ○ Overall rare ○ Physical exam findings ■ Palpate @ point of maximal impulse (PMI) to feel if it seems that the heart shifted a little

■ Elicit for a murmur ● Acyanotic Murmurs ■ Definition: No issues w/ deoxygenated blood mixing w/ oxygenated blood and therefore being pumped out into the systemic system ■ Left to right shunts ○ Ventricular septal defect (VSD) ■ Defect between the septum of the ventricle ■ Heart has higher pressure on the left side, blood from the left side of the ventricle will be shunted across from left to right into the right ventricle ● Oxygenated blood from the left side of the heart mixes with the deoxygenated blood on the right side ● That blood then going through the pulmonary artery to get oxygenated so it isn’t life threatening ■ Most common type of acyanotic & CHD defect in general ○ Patent ductus arteriosus (PDA) ■ Occurs in 5-10% of CHD ■ Fetal circulation works different when the bb is still in the womb ■ Ductus arteriosus → shunts blood away from the lungs when in utero ● Closes at 24-72 hours ■ In some kids it fails to close ● Saturated blood moves from the aorta into the pulmonary artery ● Results in increased left sided workload of the heart so down the road pts @ risk for HF ● Not necessarily dangerous unless it’s of a really large size ○ May require repair ○ Atrial septal defect (ASD) ■ Hole between the septum of the atrium ● Similar to what happens in the VSD ● Oxygenated blood moves back into the rt side of the heart w/ deoxygenated blood→ pulmonary artery → lungs→ reoxygenated ■ Relatively common ● 5-10% of kids w/ cardiac lesions have ASD, more common in females ○ Coarctation of aorta ■ Part of the aorta is basically closed off a bit, constricted ■ Often happens near the ductus arteriosus ■ Aorta gets kind of squeezed down, obstructs blood flow → increases afterload → blood supply decreased to the abd organs and lower periphery because of the decrease in blood flow ■ S/S ● Difference between BP is the arms or legs ● Pulses stronger in upper extremities vs lower extremities ○ Aortic stenosis ■ 10% of CHD ■ Narrowing entrance of the aorta ● Valve can be stenosed due to congenital reasons ■ Increased pressure in the left ventricle which will lead to hypertrophy → decreased cardiac output ○ Pulmonary stenosis* ■ Can be acyanotic if it’s mild, potential to be cyanotic in severe cases ■ 8-10% of CHD ■ Narrowing of the entrance to the pulmonary artery → obstruction → resistance in the rt ventricle → right ventricle hypertrophies → rt sided HF ● With a high enough pressure gradient it may force open the foramen ovale → patent foramen ovale (PFO) → shunt from right to left side of the heart ● Cyanotic Murmurs = deoxygenated blood is going out to the body, right to left shunts ■ Severe abnormalities of the heart, require tx ○ Tetralogy of Fallot = dis bad bad

■ 4 characteristics 1. Ventricular Septal defect 2. Rt ventricular outflow tract obstruction 3. Overriding aorta a. Aorta arising out of the right ventricle instead of left :O 4. Right ventricular hypertrophy ■ Must be ID’d right away, requires surgical repair ASAP ■ Kids have “tet spells” ● Get cyanotic, child literally becomes a smurf ○ Transposition of great arteries ■ Aorta arises from the right ventricle, pulmonary artery is coming from the left ventricle ● Desaturated blood returns to rt atrium → right ventricle → aorta → systemic system completely bypassing the lungs ● Saturated blood → left ventricle → goes to pulmonary artery and lungs ■ Assoc w/ VSD ● Allows blood to get from one side of the heart to the other, allowing for function but not compatible with life ■ In order to survive the kid will have a PFO or PDA ○ Tricuspid atresia ■ Blind pouch @ the tricuspid valve ● Rare 1-3% of defects ■ Non development of the tricuspid valve ■ Desaturated blood enters into right atrium but has no where to go, shuts from right to left through a PFO to get to left side of the heart bypassing pulmonary artery and lungs ● Deoxygenated blood goes to left side and then gets pumped out ■ Sometimes VSD present ● Allows some blood to shunt from left to right therefore getting blood to the rt ventricle that can go into the pulmonary artery ■ Require PDA or PFO to survive w/ this defect ■ Need to be recognized & surgically repaired ASAP ○ Truncus arteriosus ■ Failure of the common great vessels to divide ● Big wide opening ● Pulmonary artery and aorta mixed together ■ Deoxygenated blood mixes w/ oxygenated blood due to failure of ventricular septum ■ Mixture of deoxygenated and oxygenated blood goes to systemic system ■ Decreased o2 sat ● How low depends on the amount of blood that’s actually flowing into the pulmonary circulation ■ Must be ID’d and treated ASAP ○ Pulmonary atresia ■ Failure of pulmonary valve to develop, blind pouch ■ Blood cannot flow appropriately ■ Hypoplastic development of the pulmonary arter & the right ventricle which results in high ventricular pressure on the right side of the heart ■ Assoc w/ underdeveloped tricuspid valve ● Desaturated blood flows through the tricuspid valve into the right ventricle, cannot get to pulmonary artery, stuck, backs up into right atrium, goes through PFO ○ Deoxygenated blood from the right atrium goes to left atrium → left ventricle → aorta ■ If PDA also present, allows for blood to mix from the aorta to the pulmonary artery which allows some blood to get to the lungs and allow the child to survive ● Not good for long term survival ■ Needs to be surgically repaired ○ Hypoplastic left heart syndrome

■ Really uncommon, < 1% of defects ■ Left ventricle is severely underdeveloped ■ Only right ventricle works, assoc w/ aortic valve atresia (no development of the aortic valve ) ■ Hypoplasia of ascending aorta & mitral valve stenosis or atresia ■ Seen more in males than females, not compatible with life ■ Most children die w/in the 1st few months of life if untreated ■ Even w/ tx 5 year survival rates are low :’( ● Some parents may decide to allow child to die early in life w/in first few months vs going through the surgery and then losing them a few years later ■ ID’d in hospital when child is born, saturated blood enters left atrium but cannot flow out to the remainder of the heart ● Shunted by a PFO or ASD to get into right atrium, blood mixes w/ desaturated blood, goes into pulmonary circulation ● If there's a PDA, there may be some oxygenated blood that makes it into the systemic circulation ● Cannot live w/ just one ventricle ● Management ○ Refer to peds cardiology ○ Correct underlying problem ○ Medical management ■ Different depending on what the defect is ○ Oxygen ■ Use w/ caution in left-to-right shunt (acyanotic) ■ Changes in pressure resulting from using oxygen ○ Major consequences → HF & death ■ If HF ● Decrease afterload, work on preload until they can get the correction of the underlying problem ECG Interpretation ○ Normal conduction ■ SA node = natural pacemaker of the heart ● Gives us our regular rate and rhythm of that 60 - 100 beats per minute ● As the SA node recharges, the atria fills ■ AV node ● As it recharges ventricles fill

■ After impulse initiates in the SA node → AV node → contracts atria to pump blood into ventricles → Bundle of His → Right bundle branch → left bundle branch → purkinje fibers → causes ventricles to contract ○ WHat does PQRST mean? We just reciting the alphabet? ■ P wave → atrial depolarization ■ R wave → ventricle depolarization ■ T wave → ventricles repolarized ■ U wave → indicates recovery of Purkinje conduction fibers ○ Normal interval measurements ■ PR - 0.12-0.2 seconds, 3-5 smol squares ● Look at this in heart blocks ■ QRS - < 0.12 seconds ● Look at this for bundle branch blocks, ventricular arrhythmias ■ QT interval - 0.35-0.43 seconds ● Prolonged QT can be a risk factor for a dysrhythmia ■ ST segment ● Look at if you’re concerned for MI ○ Can be elevated or depressed ○ Calculating Heart Rate ■ # of QRS complexes in a 6 second strip x 10 = HR ■ Each small square = 0.04 seconds ■ Each large square = 0.2 seconds ● 5 large = 1 second ○ Step 1 ■ Are QRS complexes present? ● Yes → Step 2 ● No → Asystolic of ventricular fibrillation ○ Asystole they dead, no contraction ○ V fib - the ventricles are just quivering, no blood is being squeezed outta those bad boys ○ Step 2 ■ Are P waves present? *indicate Atrium function* ● Yes → proceed to step 3A ● No → step 3B ○ Step 3A ■ Are there more P waves than QRS complexes ● Yes → Conduction block ● No → Sinus rhythm ● Specific types determined by heart rate ○ Step 3B ■ Are QRS complexes wide or narrow? ● Wide = > 0.12 sec ○ Ventricular dysrhythmia ● Narrow = < 0.12 sec ○ Atrial dysrhythmia ● Cardiac Dysrhythmias ○ NSR ■ Sinus brady = HR < 60 bpm ■ Sinus tach = HR > 100 bpm ■ Originates from the SA node ○ First Degree AV Block ■ Delayed conduction through the AV node results in PR segment > 0.2 seconds ■ > 0.3 is a significant delay ■ Pts w/ 1st degree, asymptomatic, observe them ● Increased risk of developing afib

○ Second Degree AV Block T1 “Movitz I” or “winky block” ■ Progressive prolongation of the PR interval ■ Becomes so great a P wave is dropped ■ Reversible conduction block in the AV node secondary to ● Beta blockers, calcium channel blockers, increased vagal tone ● Pts are also asymptomatic frequently ● Monitor, if due to a med, stop the med ○ Second Degree AV Block T2 Movitz II“ ■ Intermittent non-conducted P wave w/out any warning ■ PR interval remains constant but it just be dropping p waves ■ Occurs below the AV node, somewhere in the bundle of his/other bundles ■ Common in pts who have had an anterior MI, septal infarct, fibrosis ● Autoimmune disorders ex. Lupus, Lyme, myocarditis ● Medications, electrolyte imbalances ■ Can lead to severe bradycardia and instability ● High risk of going into complete heart block, risk of asystole ■ Refer for a pacemaker!!! ● Immediate referral & eval for pacemaker, not managed just in primary care ○ Third Degree AV Block or Complete heart block ■ Complete absence of AV nodal conduction ■ P waves are not related to the QRS, complete dissociation ● Its complete chaos, waves are running amok ■ Supraventricular impulses are not conducting into the ventricles ■ If there is ventricular conduction, the QRS will appear ● Some type of junctional escape rhythm ● Ventricles are conducting independently of the atrium ■ Seen after an MI ■ BB, Ca channel blockers, adenosine & amiodarone can also cause this ■ High risk of asystole, vtach and death ■ Refer for pacer!!! ■ Not likely going to see in primary care, important to be able to know if you have a pt who has a hx of 3rd degree heart block ○ Wolf Parkinson White Syndrome ■ Can been seen from a newborn stage throughout life ■ Extra electrical pathway btw the heart’s upper and lower chambers causing a rapid heartbeat ■ Funky notch in the QRS segment ⇒ “Delta wave” ■ Pt may complain of palpitations or tachycardia ● Rapid fluttering heartbeat, dizziness, lightheadedness, SOB, fatigue, anxiety ● Possibly chest pain, dyspnea ■ In an infant may have cyanosis (grey blue skin), signs of poor feeding, rapid breathing & restlessness ■ Urgent referral to cardiology ● Ablation ○ Atrial Fibrillation ■ Overview ● Most common dysrhythmia ○ Second most common rhythm after sinus rhythm ○ As people age, becomes more common ● Risk Factors ○ Structural changes, Congestive HF, valvular failure, previous MI, Sleep apnea, obesity, alcohol, stimulants ex. tobacco caffeine, meds ex. decongestants ○ Idiopathic but people w/ HTN or valvular heart dz @ higher risk ■ Hyperthyroidism and other disorders as well ● PCP role ○ ID afib, determine risk of stroke, initiate anticoags ○ Get an ECHO!

○ Consider antiarrhythmic meds ● Types: ○ Paroxysmal : Occurs for < 7 days & self terminates ○ Persistent: > 7 days or resolved w/ cardioversion after 48 hrs ○ Permanent: No further efforts are being pursued to restore NSR ■ What’s Happening? ● No p waves, it’s just fibrillation ● Irregularly irregular, no SA node stimulation, ectopic beats, atria are simply quivering, do not contract ○ Electrical pathway disrupted ○ Ventricular contraction is all good ● Blood pools in atria ⇒ increased risk for blood clot, stroke! ● Rate is fast due to the # of stimuli, can be over 110 ■ Management ● Calculate CHADS-Vasc 2 score to see what their risk of stroke is ○ C HF (1) ○ H TN (1) ○ A ge > 75 (2) ○ D M (1) ○ S troke/thromboembolism hx (2) ○ V ascular Dz (1) ○ A ge 65-74 (1) ○ S ex - female (1) ■ Depending on the score, treat them accordingly w/ an anticoagulant ■ Low risk = 0 No anticoag, full dose ASA only ■ Low-mod = 1 either anticoag or full dose ASA ■ Mod-high = 2+ anticoag recommended! ■ Blood thinners ● Warfarin - old gold standard, narrow therapeutic index ● Direct-acting oral anticoagulants (DOACs) ○ Dabigatran, Xarelto, Eliquis ● See if they need to be on an antiarrhythmic ○ Possibly refer to cardio for a TEE & cardioversion ■ New onset afib ■ Chronic? No cardioversion ○ First line meds ■ Beta blockers ex. Metoprolol ● If rate and rhythm are controlled, manage in primary care. If not → refer! ○ Can be treated w/ an ablation if pts having a lot of problems ■ Get an ectopic pacemaker & they stop it so it can go back to the normal function ○ Atrial Flutter ■ Sawtooth pattern!! 4 flutters to 1 QRS conduction ■ Results from an abnormality of conduction in the atrium ● Ventricles working normally ■ Can be idiopathic, can occur w/ people who have cor pulmonale ● Heart dz, ischemic heart dz, HTN, hyperthyroidism, valvular heart dz, congenital heart dz ○ Supraventricular Tachycardia (SVT) ■ Impulses above the ventricles in the atria, over 100 bpm ■ Proximal, self limiting, too fast to differentiate underlying rhythm ■ Can be slowed w/ adenosine in the ER ● If outpt, try vagal maneuvers to slow it down ○ If not successful → ER!!! ○ Ventricular Tachycardia ■ Wide QRS segment > 0.12

■ 3 PVCs in a row = run of VTACH ■ Can be life threatening if it continues ● Need implanted cardiac defibrillator placed!! ■ At risk - Pts w/ structural heart dz, valvular heart dz, HF, CAD, hx of MI ■ Symptoms ● Dizziness, lightheadedness, chest pain, neck tightness, SOB, syncope, other cardiac symptoms ● Antiarrhythmic Agents ○ Goal is to restore rhythm & conduction, Prevent more serious dysrhythmias ○ Some are only going to be started after cardio consult, sometimes even w/ an electrophysiologist ■ Often the pt needs to have a stress test or ECHO before starting these meds ■ If it’s afib in the primary care setting, may start them on metoprolol w/o consult ○ Class 1: Na Channel blockers ■ Flecainide ○ Class II: Beta antagonist agents ■ Beta blockers ex. Metoprolol ○ Class III: Potassium channel blockers ■ Sotalol ○ Class IV: Calcium channel blockers ■ Verapamil ○ Amiodarone ■ One of the most effective antiarrhythmics ■ Effects across all classes, Na, K, Ca, Beta ● Palpitations ○ Overview ■ “Fluttering” or “flopping” in chest ■ 16% of primary care visits ● 2nd most common cardio complaint ■ Cardiac and noncardiac etiologies, figure out what the origin is! ■ Requires thorough H&P ● Do they have a hx of CVD? Do they have palpitations while at work, affect their sleep? ● HX of panic attacks or anxiety ● Meds they’re on ● Impacted by positions like leaning forward? ● Do a full cardiac exam, listen for murmurs, ID any irregular rhythms, order any subsequent dx tests ■ Most common causes ○ Cardiac Causes - high risk of sudden death :O ■ Atrial fibrillation/flutter ● 16% afib ■ Premature atrial contractions ■ Cardiomyopathy ■ Long QT syndrome ■ Supraventricular tachycardia ● 10% of cases ■ Valvular heart disease ■ Premature ventricular contractions ■ Ventricular tachycardia ● 2% of cases ■ Structural heart dz or alveolar heart dz ● 3% of cases ○ Noncardiac Causes ■ Anxiety/stress ● 31% of cases ■ MEds and illicit substances are 6% of cases ■ Anemia

■ Beta-blocker withdrawal ■ Caffeine ■ Exercise ■ Fever ■ Medications ■ Pregnancy ■ Thyroid dysfunction ○ Dx Testing ■ Labs ● TSH, CBC, BUN, Creatinine, electrolytes ■ 12-lead EKG (electrocardiogram) ■ 24-hour Holter monitor ■ Event monitor that’s for days on end ■ Exercise stress test ● Esp if they’re having exertional symptoms ■ Tilt test ● If having syncopal episodes ■ Transthoracic echocardiography ○ If not able to figure it out → refer to cardio ○ Tx based on underlying cause COPD & Asthma Chronic Cough ● Overview ○ Cough lasting longer than 8 weeks ○ Cough most often due to viral URI or nonviral cause (ex. Asthma, exposure to pollutants) ○ Excessive & chronic cough can result in numerous complications ● Classification of Cough ○ Acute : Lasting < 3 weeks ○ Subacute : Lasting 3-8 weeks ○ Chronic : Persisting beyond 8 weeks ● Causes (w/ normal chest x ray) ○ Corticosteroid-responsive eosinophilic airway dzs (asthma, cough variant asthma & eosinophilic bronchitis) ○ Upper airway cough syndrome (previously referred to as postnasal drip syndrome) ○ GERD ● Presentation ○ H&P can establish the cause of cough ■ Obtain thorough hx of cough, PMHx, meds, smoking hx, occupational exposure ■ Perform thorough exam, VS ● HEENT, pulm, cardiac, abd ● Dx ○ Chest x ray ○ Bronchoscopy ○ PFTs ○ CT scan ○ Barium ○ 24 hr pH monitoring ○ Esophagography ○ Cardiac studies ○ GERD med trial ● Diff Dx ○ Asthma ○ Upper airway cough syndrome (post nasal drip syndrome) ○ GERD

○ Perennial rhinitis ○ Irritants ○ Meds ○ Vasomotor responses ○ Chronic sinusitis ● Management ○ Tx is either: ■ Antitussive ● To prevent, control, or eliminate cough ■ Protussive ● To make cough more effective & productive ○ Eliminate triggers (smoke, ACEI, allergens) ○ Demulcents, opiates, GERD trial of PPIs, if purulent exudates ○ Treat underlying cause of cough Asthma ● Overview ○ Seen frequently in primary care ○ Chronic dz ■ Chronic reversible inflammatory disorder of the airways ■ May start in childhood and becomes milder as they grow older ■ Adults can present w/ s/s consistent w/ asthma and be newly dxd ● Chronic cough, wheezing, etc ○ Increasing incidence of asthma ■ Prevalence higher in black children ● Minority children receive less preventive care ○ Ambulatory visits ○ Controller meds ○ Emergency evaluation/ treatment is indicated for persons with signs and symptoms suggestive of respiratory compromise including: ■ Respiratory rate > 30/ min ■ Pulse rate > 120 beats per minute ■ O2 saturation (on room air) < 90% ■ Peak expiratory flow (PEF) < 50% predicted or best, drowsiness, confusion, or silent chest. ● What is it? ○ Chronic inflammatory disorder of the airways ■ Characterized by increased responsiveness of the tracheobronchial tree to various stimuli ■ Bronchioles (small airways) ■ Inflammation, mucus buildup → leads to narrowing of airways → obstruction of airflow → Wheezing SOB, chest tightness & cough ○ Asthma attacks can vary from mild to severe ○ Various triggers ■ Allergens, infections, exercise, abrupt changes in weather ● Allergens include house dust mites, cockroaches, indoor molds ● Saliva/dander of cats/dogs ● Outdoor seasonal molds, pollens ● Food allergy ■ Exposure to airway irritants (ex. Tobacco smoke)

■ Rapid changes in temperature, barometric pressure ■ Endocrine factors ■ GERD ○ Persistent inflammation leads to ■ Airway remodeling ● Occurs 2ndary to persistent fibrotic changes starting in childhood - different phenotypes, depending on age of onset ■ Acute bronchoconstriction ■ Airway edema ■ Mucous plug formation ● Establishing Dx ○ Med hx ■ Family hx, hx of allergies, eczema ■ Conditions associated w/ asthma - GERD, sinusitis, chronic OM ■ Recurrent “bronchitis” or PNA, seasonal or continuous symptoms ○ Symptoms - Get a detailed history of symptoms!! ■ Is the pt presenting w/ episodic symptoms? Do they seem to be consistent w/ the fact there is some type of obstruction & is the obstruction @ least partially reversible? If not, NOT asthma! ■ Cough is the most common symptom!! ■ Wheezing, hx of cough, possible worse w/ exercise or animals, allergies, stress makes it worse, worse at night, wakens pt from sleep ■ Breathlessness & anxiety w/ wheezing ● Increased work of breathing/signs of distress ■ Diminished breath sounds ■ Every time they have a URI, they wheeze ■ Between episodes s/s may improve or completely resolve ● Symptoms vary from mild to severe w/ varying effects on activity ○ Physical exam ■ Look at upper resp system, lungs, chest, skin for changes that might be consistent w/ decreased O2 capacity ■ Clinical Hallmark → Episodic wheezing assoc w/ dyspnea, cough & sputum production ■ 4 objectives of exam 1. Dx & diff dx 2. Assessment of asthma severity 3. ID of adverse effects of meds 4. ID concomitant med problems ○ Dx ■ DX of exclusion ● Episodic symptoms of airflow obstruction ex. Wheeze, cough, SOB ● Evidence that airflow obstruction is @ least partially reversible (trial of bronchodilator) ● Exclusion of other conditions from the diff dx ■ Peak flow meters ■ Spirometry (peak expiratory flow rate (PEFR) & FEV1) ● Tells us 1. Is there an obstruction? 2. Is it reversible ● Forced Expiratory Volume (FEV1) ● Then admin SABA ex. Albuterol nebulizer ● Repeat spirometry & look for signs of reversible obstruction, if FEV1 improved this is considered a hallmark sign ■ Additional tests ● CBC if secondary infection ● Allergy eval ● Sweat test ● Pulmonary function tests ■ Pulse Ox @ every assessment

■ *Rarely dx before 12 mo due to high rates of viral bronchiolitis * ● Diff dx - think why are they SOB, recurrent wheezing, chronic cough? ○ Upper respiratory ■ Croup ■ Acute bronchiolitis, laryngotracheobronchitis ■ Laryngeal and/or Vocal cord dysfunction ○ Lower respiratory ■ PNA ■ COPD ○ Airway Obstruction → foreign body aspiration ○ Tracheal compression, PE, pulmonary abnormalities ○ Cardiovascular ■ Valvular Dz ■ Cardiomyopathy ■ CHF ■ Congenital issues ○ GI - GERD ■ Gerd from constant reflux can cause wheezing & cough ○ Cystic Fibrosis/alpha-1 antitrypsin deficiency ○ Cough related to meds ● Classification of asthma severity ○ Depends on symptoms, recurrences, need for meds, pulmonary function measure ■ Intermittent ■ Mild persistent ■ Moderate persistent ■ Severe persistent ○ May have mild, moderate, severe exacerbations @ any level ○ Early phase responses (EAR) ■ Activation of mast cells/mediators ■ Bronchoconstriction key feature ■ Starts in 15-20 min; resolves in 1 hr after removal of allergen ○ Late phase response ■ Prolonged inflammatory state ■ Follows EAR w/in 4-12 hours ■ Airway hyper-responsiveness more severe ■ May last hours to weeks ○ Exercise-induced bronchospasm ■ Airway narrowing during or minutes after vigorous exercise ■ May be only trigger for some ○ Many w/ asthma have allergic component ○ Whether hyper-responsiveness present @ birth or acquired is unknown ○ Genetic predisposition to atopy strongest identifiable predisposing risk factor ● Determining risk ○ What is their risk of having high morbidity or mortality? ○ Assess how controlled their asthma is ○ Symptoms ■ Nighttime awakenings ○ How often are they using Short acting beta agonist use? ■ More than twice a week ⇒ NOT controlled ○ Lung function ■ Assess through spirometry ○ Exacerbations requiring systemic steroids ■ How often are they having those exacerbations ■ If they have to be admitted to ICU or require ventilator support HUGE RISK ● Monitoring Asthma Control

○ Signs & symptoms ○ Lung function ■ Determine functional status ● Look at the spirometry test! Does it look like its improving ■ Number of exacerbations ■ Asthma Control Test (ACT), Asthma Control Questionnaire, others ● Allows assessment of changes, responses to tx ○ Well vs poorly controlled ■ Well controlled Asthma: Symptoms < 2 days/wk , Use SABA < 2days/week ■ Poorly Controlled: Symptoms > 2 days/week, need step up in meds ○ Pharmacological regimen ■ Tailor tx based on where the patient’s at ○ Patient satisfaction ■ How happy are they with where they are? Are they able to complete ADLs ○ Avoidance of triggers ● Successful Management ○ Education ● Chronic disorder, what to expect, what it means to have inflammation in the airways, why it’s important to tx even if not symptomatic ● If obstruction is not managed, it can lead to chronic long term inflammatory changes w/in the lung ● ID triggers ex. Pets, environmental allergies & how to avoid them ■ Asthma action plan!! ● Green zone ○ Asthma symptoms are great, things are going well ● Yellow zone ○ URI ○ Empowers pts to tx themselves in the setting of the home & then also when to contact for further management ● Red zone ■ Know how to ID symptoms ● Watch for changes indicating a need for change in therapy/when to seek emergency care ■ Teach them about using peak flow! ● Do it every day they’re going to know what their normal is & when things are starting to decline ○ Shows what the level of inflammation and obstruction is throughout the lungs @ any given time ● Can help them ID exacerbations early on ■ What their medications do, when do they use them ○ Environmental control ■ Parents smoke in the house? They have to smoke outside! No cancer sticks in the house!! ■ Reduce environmental/allergen exposures Avoid wood burning stoves, limit perfumes, avoid cleaning products, grass pollens ○ Treat Rhinitis, sinusitis, GERD

○ Appropriate Pharmacological Therapy ■ Rescue (reliever) vs maintenance (controller) ● Long acting → inhaled corticosteroids (ICS), leukotriene modifiers, long acting beta agonists (LABA) ○ Add-on controller medications include long-acting anticholinergic, Anti-IgE, Anti-IL5 and systemic corticosteroids ● Short acting → short acting B2 agonist bronchodilators (SABA), steroids ○ SABAs - Ventolin, ProAir ○ Low dose ICS/formoterol ○ Short acting anticholinergics ● **Systemic steroids may be needed @ any time*** ● MDIs/spacers or nebulizers for B-agnostis ○ Dry powder inhalers do not need spacers ■ Other meds ● Cromolyn sodium → decreases inflammation ● Omalizumab → prescribed by pulmonologist ■ Step Therapy ● Beginning to intermittent s/s start w/ SABA ○ Using it too often? Start on a low dose ICS! ○ Still not enough? LABA or medium dose ICS! ○ Still not cutting it? LABA w/ high dose ICS ● Exacerbation ○ Oral corticosteroids ● The Steps! ○ Step 1 ■ Reliever medication: As needed short-acting β2-agonist (SABA) for relief of symptoms. ○ Step 2 ■ Reliever medication: As-need short acting β2-agonist (SABA). ■ Preferred controlled choice: low dose ICS. ○ Step 3 ■ Reliever medication: As-needed SABA or low dose ICS/formoterol. ■ Preferred controller choice: Low dose ICS/LABA. ○ Step 4 ■ Reliever medication: As needed SABA or low dose ICS/formoterol ■ Preferred controller choice: Med/high ICS/LABA. ○ Step 5 ■ Consultation ○ If well controlled for 3 months, may “step down” ○ Early management of exacerbations ■ Pt needs to be aware of what to look for so they can initiate self management @ home based on the plan of care ■ What S/S they need to look for ■ When do they contact their PCP ○ Yearly flu vaccine ○ Managing special situations ■ Preggo pts w/ asthma ■ Pts going in for surgery

● Complications ○ Mild secondary respiratory infections ○ Respiratory distress to arrest ○ Chronic high steroid use can lead to growth retardation ● Referral Guidelines ○ Diagnostic uncertainty ○ Risk of asthma-related death → refer early!!! ○ Medication adverse effects ○ Lack of response to treatment after 3-6 mos, Poorly controlled asthma ○ Possible phenotype-driven treatment Asthma Exacerbation ● Overview ○ Referred as an “asthma attack” ■ Inflammation of the bronchioles & excess mucus causing obstruction, continues to get worse → more mucus, more constricted airway, tightened muscles ■ Immunohistopathologic response ○ Can lead to hospitalization or intubation ○ Be on alert for very serious symptoms ○ Collect hx, if they have been hospitalized before due to asthma, they are at high risk for mortality ■ Be extra careful with these pts! ○ Onset requires: genetic predisposition, exposure to environmental factors ● Presentation ○ Severe wheezing , inspiratory or expiratory ○ Prolonged expiratory phase ○ Increase in cough, reports of dyspnea, rapid breathing ○ Complaints of a tight chest or neck muscles ○ Difficulty talking, feeling anxious or panicked ○ Pale, sweaty face ■ Cyanosis ○ Leaning over in a tripod position to get air → indicates severe distress! Go to the ER!! ● Triggers ○ Allergies ex. Pollen, grass ○ Smoking ○ URI ■ Respiratory virus, mycoplasma, chlamydia ○ Psychological stress ● Asthma action plan!

○ Acute exacerbations ■ Based on severity of episode → response to initial tx determines subsequent treatment ● Start at step of initial severity ■ **ICS w/ LABA in some cases** ● New guidelines - use both ○ Add PO steroid burst, prednisone or prednisolone (for peds pts, wt based) ■ Ex. 50 mg once a day for 5 days for adults ○ SABA Q 4 hours ■ When they’re bad make it a nebulizer treatment ○ When it’s a child, if they get a URI → Yellow zone! ■ Corticosteroids, bronchodilators, anticholinergics ■ DuoNeb instead of their inhaler ■ Nebulized budesonide, prednisone ■ Once s/s start to go away, go back to normal maintenance meds ○ Drugs given in more severe asthma when hospitalized ■ Magnesium sulfate IV ■ Ipratropium oral inhalation ■ Epinephrine SQ or Im ■ Heliox to improve drug delivery in airways ● Status asthmaticus ○ ER for continuous nebulization Atopic Triad ● The Triad!! “Asthma Triad” used to be called “Samter’s triad” ○ Asthma, Allergies, Eczema ○ If you got it, you’ve got a more severe asthma situation ● Hx ○ Ask if they have symptoms of eczema - rash in flexor surfaces or have been dx w/ eczema in the past ○ Allergic Rhinitis ● Management ○ Need inhaler more, worse situation for these kiddos - more at risk for severe exacerbations ● Exam ○ Atopic dermatitis, nasal polyps ○ Can have an aspirin sensitivity or any NSAIDs! ■ Avoid as this kid would have increased resp s/s Chronic Obstructive Pulmonary Disease (COPD) ● Overview ○ Preventable & treatable dz characterized by airflow limitation ○ Used to describe 2 related lung dzs: Chronic Bronchitis & emphysema ■ Does not include other obstructive lung dzs such as asthma ○ Predominantly a smoker’s disease that clusters in families & worsens w/ age ○ Chronic progessive disease of the lungs, characterized by irreversible airflow limitation & abnormal inflammatory response in the lungs ■ Includes both chronic bronchitis & emphysema ■ airflow limitation that is not fully reversible, usually midlife onset ■ Usually progresses & associated w/ abnormal inflammatory response to particles or gasses ○ Destruction and remodeling of the airways & alveoli ■ Airway hyperresponsiveness, excess mucus production in the bronchioles, extends into smaller bronchioles ■ Alveoli involved in emphysema ● Alveoli are damaged, no longer have elastic recoil ● Pts cannot drive the air out of the alveoli ● Trouble inhaling and exhaling ○ Causes

■ Most common cause of COPD → smoking ■ Occupational exposure ■ Alpha-1 antitrypsin deficiency ● Consider in younger pts who have never smoked, esp if there’s a family hx of it ■ Asthma ○ Presentation ■ Chronic progressive cough, dyspnea on exertion, sputum production ● Dyspnea is persistent, progressive ● Worse w/ exercise ■ Usual Onset middle age ○ Emphysema vs Chronic Bronchitis ■ Chronic bronchitis ● Pts more likely to be obese ● Frequent cough w/ more sputum production ○ Use accessory muscles ● Presentation ○ Coarse bronchi & wheezes ○ More likely to have rt sided HF or cor pulmonale ■ Edema, cyanosis ■ Emphysema ● Pts more likely to be thin w/ barrel chest ● Cough but w/ little sputum ● Presentation ○ Pursed lip breathing, use accessory muscles, tripod position ○ Hyperresonance, wheezing, heart sounds distant ● Hx ○ Age of onset, smoking history ○ Chronic cough, Sputum production, Wheezing, Fatigue ○ Pattern of symptoms ■ Progresive dyspnea, worse over time ■ Worse w/ exercise ○ Occupational or environmental exposures ○ History of frequent respiratory infections ○ Impact of symptoms ■ Are they missing work? Impacting ADLs? Depression? Economic impact? ○ History of respiratory diseases or allergies ○ Family history of respiratory disease ○ Social history ● Exam ○ Often normal until the disease becomes more advanced ○ Use of accessory muscles, intercostal muscle retraction ■ Hyperinflated “barrel” chest ■ Audible inspiratory crackles, forward sitting position ○ Auscultation - reduced breath sounds, wheeze ■ Heart sounds loudest in epigastrium ○ Pursed lip breathing, central cyanosis, prolonged expiration ○ Skin changes! ● Tobacco stains on fingers, clubbing of the fingernails ○ Reduced cricosternal distance ○ Intercostal indrawing during inspiration ○ Cardiac apex not palpable, loss of cardiac dullness on percussion ■ Right ventricular hypertrophy (cor pulmonale) ○ Inward movement of lower ribs on inspiration (Low flat diaphragm) ● Modified medical Research Council Dyspnea Scale & COPD Assessment Test ○ mMRC Breathlessness Scale

■ 0 - only get breathless w/ strenuous exercise ■ 1 - SOB when hurrying on level ground or walking up a slight hill ■ 2- On ground level I walk slower than people of the same age b/c of breathlessness or have to stop for breath when walking at my own pace ■ 3- I stop for breath after walking about 100 yards or after a few minutes on level ground ■ 4- I am too breathless to leave the house or I am breathless when dressing ○ COPD Assessment Test (CAT) ■ 8 item questionnaire, helpful in determining how severe their dz is & helps w/ determining what their management plan is going to be ● Dx ○ Spirometry ■ Give a SABA before, have them do the spirometry, document FEV1 ■ FEV1 = amount of air the pt can expel w/in 1 second ● < 80% = COPD ■ FEV1/FVC if it = < 0.7% → Dx of COPD ● Confirms airflow limitation, not reversible obstruction ○ Pulse ox ○ COPD Assessment Test (CAT) ○ CBC ■ Look for anemia of chronic dz ■ May see polycythemia as a response to having lower O2 levels ■ Eosinophils (respond to ICS) ○ Alpha-1 antitrypsin deficiency ■ Check if patient does not smoke, young ○ Chest X ray ■ Helps support dx ■ Hyperinflation of the lungs, flattened diaphragm ○ Blood gas measure = O2 < 92% ● Diff dx ○ Asthma ○ Chronic sinusitis or chronic rhinitis from allergies or postinfectious states ○ Lung cancer ○ TB ■ If they have hemoptysis, fevers or night sweats ○ Heart failure ○ GERD ○ Neoplasms ○ Cystic Fibrosis ○ Interstitial lung dz ○ Heart dz, HF ■ Ex. mitral stenosis or those causing chronic pulmonary edema ○ Bronchiectasis ○ Side effects of drugs (ex. ACEI, BB) ■ BB exacerbate SOB in asthmatics ● Groups ○ Group A = Bronchodilator ■ 0 or 1 mod exacerbations, not leading to hospital admin ■ mMRC 0-1 CAT < 10 ○ Group B = A Long acting Bronchodilator (LABA or LAMA) ■ 0 or 1 mod exacerbations, not leading to hospital admin ■ mMRC >/= 2 CAT >/= 10 ■ LAMA = Tiotropium ○ Group C = LAMA ■ >/= 2 mod exacerbations or >/= 1 leading to hospitalization ■ mMRC 0-1 CAT < 10

○ Group D = LAMA or LAMA + LABA or ISC + LABA ■ >/= 2 mod exacerbations or >/= 1 leading to hospitalization ■ mMRC >/= 2 CAT >/= 10 ■ Consider LAMA + LABA if highly symptomatic ex. CAT > 20 ■ Consider ICS + LABA if eos >/= 300 ○ GOLD Grading ■ Grade 1-4 based on FEV1 ● Grade 1 > 80 ● Grade 2 50-79 ● Grade 3 30-49 ● Grade 4 < 30 ● Management ○ Goal: Improve dyspnea, improve QOL, slow progression of dz & reduce mortality ○ Smoking cessation** ■ Reduces rate of FEV1 decline & mortality ■ Counseling ■ Referral ■ Medications ● Nicotine replacement, varenicline, bupropion (Chantix) ○ Vaccination ○ Pulmonary rehabilitation ■ For mod to severe dz ■ Reduces dyspnea, increases exercise tolerance & ability ■ Lead to better QOL ○ Education & support ■ Exercise, stay active ■ Nutrition ● Frequently these pts have trouble eating ● Focus on high caloric food, high protein, ex. Boost! ■ How to manage dz ■ Med compliance, proper inhaler techniques, when to seek medical care ■ Exacerbation management ● Pursed lip breathing when they become dyspneic ○ Screen for depression/anxiety, osteoporosis ■ Osteoporosis esp if they’re on PO steroids ○ Oxygen therapy

■ Indications for long term oxygen ● RA ABG = O2 </= 55 mm Hg or 56-59 w/ cor pulmonale or signs of tissue hypoxia ● RA O2 sat </= 88% or </= 89% w/ cor pulmonale or signs of tissue hypoxia ● Nocturnal oxygen sat </= 88% (use O2 @ night only) ● Exercise hypoxemia w/ arterial partial pressure of oxygen </= 55 mm Hg, or O2 sat </= 88% (use O2 only w/ exertion) ■ Wear @ least 15 hours a day , can be used for nocturnal hypoxia or hypoxia assoc w/ exercise ○ COPD Meds → LABAS, LAMAS ■ Inhaled meds ● Bronchodilators ○ SABA ○ SAMA ○ LABA ○ LAMA ● Inhaled Corticosteroids (ICS) ○ More often used in pts who have asthma & COPD ● Metered dose inhaler (MDI) ○ Requires coordination ● Dry powder inhaler (DPI) ○ Pts have more control over that ● Soft mist inhaler (SMI) ■ Oral meds ● Methylxanthines ○ Ex. theophylline ■ Not really recommended because there are other safer classes of meds w/ less SEs ● Phosphodiesterase-4 PDE-4 Inhibitors ○ Used for pts who continue to have symptoms despite being on a long acting bronchodilator & ICS ● Corticosteroids ○ During acute exacerbations ○ Vaccinations ■ Flu, PNA ○ Referral to palliative care in more advanced stages ○ Refer to Pulmonology in pts w/ more severe symptoms ■ Consult recommended for the initial dx & management of pts w/ significant change in condition or a failure to improve w/ prescribed therapies ● Follow Up ○ Revew symptoms, exacerbations ○ Assess ■ Inhaler technique & adherence ■ Non-pharm approaches (Including pulmonary rehab & self-management education) ○ Adjust ■ Escalate ● Ex. they’re on a LABA, consider adding a LAMA ■ Switch inhaler device or molecules ● Think of the cost of meds too! ■ De-escalate COPD Exacerbation ● Symptoms ○ Worsening symptoms from baseline ○ Worsening cough, dyspnea and/or sputum production ■ Change in color of sputum ○ Wheezing, chest tightness ● Etiology

○ Viral infections - most common ○ Bacterial infections ex. PNA ○ Pollutants ○ Med noncompliance ● Exam ○ Tachypnea, wheezing, rhonchi, diminished breath sounds ● Diff dx ○ HF, PE, asthma, PNA, pneumothorax ● Criteria for classification of exacerbation ○ Based on: Increased sputum, increased sputum purulence, dyspnea & cough ○ Mild ■ 1 of those symptoms w/ URI ■ SABA prn ○ Moderate ■ 2 of the symptoms ■ SABA, oral steroids 5-7 days, antibiotic if indicated ○ Severe ■ 3 of the symptoms ■ Hospitalize ● Work Up ○ O2 sat ○ Chest x ray to r/o PNA or pneumothorax ○ CBC ■ If suspecting infection ○ BNP ■ If considering HF ● Tx ○ Hospitalization for pts who have severe s/s or considerable comorbidities or inadequate home support ○ Outpt ■ SABA, oral corticosteroid (Prednisone 40 mg Q 5 days) ■ Antibx ● If increased purulent sputum in addition to one of the other two symptoms (cough, fever) ● Tetracycline, Augmentin, macrolide for 5 days ■ Eval if the pt needs to step up the tx for their daily maintenance meds Chronic GI Problems GI Red Flags! ● Rectal bleeding, Wt loss, unexplained fever & anemia ○ Pt may report hx of anemia or seen on CBC ○ Could point to IBD ○ Pt > 50 yo? Consider GI malignancy ● Nocturnal diarrhea ○ Ulcerative colitis ● Acute bowel change > 50 yo ○ In shape, frequency, caliber of BM ● Abd pass ● Persistent vomiting ● Jaundice ○ Think liver! ● Dysphagia or odynophagia ○ In older pt w/ ongoing GERD symptoms → GI malignancy ex. Esophageal cancer ● Perianal dz ○ Abscess, fistula ○ Can occur w/ IBD, esp Crohn’s

● Arthritis assoc w/ GI problems → IBD ● Bilious emesis, hematemesis ● Family hx of colon ca ● In kids ○ Poor weight gain or linear growth ○ Absent pubertal changes Irritable Bowel Disease ● IBD is a disease of remission and exacerbation. ○ Cigarette smoking exacerbates CD, and patients should be encouraged to stop smoking. ○ A healthy lifestyle and stress management should be encouraged. ○ Adherence with the prescribed treatment regimen and regular follow-up are the two most important strategies patients can implement to maximize their health. ○ Patients with IBD are at higher risk for colon cancer and need regular colon cancer surveillance. ● Immediate physician consultation is indicated for patients who develop weight loss, nausea, vomiting, severe abdominal pain, significant blood loss, and malnutrition & other systemic symptoms. Crohn’s Disease ● Overview ○ Chronic inflammation of the GI tract ■ Can affect anywhere in the GI tract from mouth to anus ○ Common → terminal ileum/colon ● Symptoms depend on location of diseased area ○ Rectal bleeding, abd pain ● ■ Patchy inflammation ● Skip lesions ■ “Transmural inflammation” involves whole thickness of the colon ● Fistulas and fissures common ○ Associated w/ extraintestinal s/s ○ Cause ■ Genetic, something in the environment triggers development of the dz ■ Esophageal disease in 29%, perianal dz common ○ The presentation is affected by site involvement and whether the disease is only inflammatory or also complicated by fibrostenosis or penetration of the bowel wall, creating fistulas, abscesses and perforation ○ The majority of patients with CD have disease in the small intestine (ileitis or regional enteritis), but some will have inflammation that involves both the ileum and colon and a small number will have disease only in the colon ● Symptoms ○ Abd pain ■ May or may not have diarrhea or constitutional symptoms ■ Diarrhea more common in kids ● May or may not be bloody ● Presents longer than 4 weeks in adults, 6 weeks in kids ○ Weight loss, fatigue ○ Growth failure, Delayed puberty in child ○ Fatigue ○ Perianal diz: fissures, fistula or abscess ○ Intestinal obstruction ● Signs ○ Abdominal tenderness ■ Could be localized or diffuse lower abd tenderness ○ Stomatitis ○ Eye inflammation ■ Iritis, episcleritis ■ Seek medical care!

○ Mouth Ulcer ■ “Canker sores” ○ Skin ulcers/sores, lesions ■ Erythema nodosum - painful erythematous swelling that usually occurs on the extremities ■ Psoriasis ○ Vomiting ■ Fever, weight loss, decreased appetite ○ Joint pain & swelling ■ Arthritis ○ Liver & bile duct inflammation ○ Intestinal ■ Diarrhea, abd pain, cramping, ulcers in digestive tract, rectal bleeding ● Exam ○ Weight/height: assess for weight loss or growth failure in child ○ Skin: erythema nodosum, psoriasis ○ Eyes: uveitis, episcleritis ○ Mouth: ulcers ○ Joints: edema, erythema, decreased range of motion ○ (ROM) ○ Gastrointestinal (GI): tenderness, mass ○ Rectal: fissures, fistulas, abscesses ● Evaluation: Adult ○ Labs ■ CBC ● Look for anemia ■ CRP, Sed rate → elevated ● Normal does not r/o ■ LFTs → often AST and ALT elevated ■ Glucose, BUN, creatinine, vitamin D, folate, iron, & B12 ■ Stool for ova and parasites, Clostridium difficile (C. diff) ■ Fecal calprotectin ● Sensitive test ● Positive w/ Crohn’s and other IBD disorders ○ Not specific can be elevated in Celiac ○ Imaging ■ CT scan: inflammation, perforation, abscess ● Used in acutely ill pts ○ Colonoscopy ■ Cobblestoning (patches of normal mucosa & inflamed mucosa) ■ Can get a biopsy ■ Inflamed terminal ileum ● Evaluation: Child ○ Labs: same as adult ○ Refer for Ileocolonoscopy & esophagogastroduodenoscopy (EGD) ○ (EGD) with biopsy ○ Small bowel imaging ■ Magnetic resonance enterography ■ Wireless capsule endoscopy ● Management & Education ○ GI referral ■ Initial dx & management ○ Assess severity ○ Education ■ Compliance ■ Medication adverse effects

■ Lifestyle ● Diet, exercise, nutrition to prevent deficiencies ■ Support ■ Vaccinations ● Especially if on immunosuppressants ■ Complications ● Obstruction ○ Medications ■ GI determines, depends on pts age, level of inflammation and comorbidities ■ Corticosteroids, immunomodulators, biologics Ulcerative Colitis (UC) ● Chronic Disease - Diffuse inflammation of rectal/colonic mucosa ○ Involves rectum in 95% of cases ○ Multifactorial basis – heredity, diet, environment, immunologic, ineffective mucosal integrity ○ Incidence increased in developing nations ● Symptoms ○ Abdominal pain - intermittent or constant cramping pain ○ Bloody diarrhea ■ If colon involved ○ Urgency, Tenesmus ○ Weight loss ○ Delayed growth & sexual maturation in kids ○ Pain w/ defecation ○ Nocturnal defecation ○ Fever (severe flare) ● Extraintestinal Symptoms ○ *Hyperactive bowel sounds* ○ Eyes: Episcleritis, Uveitis ○ Kidneys: Stones, Hydronephrosis, fistulae, UTI ○ Skin: Erythema nodosum, pyoderma gangrenosum ○ Mouth: Stomatitis, aphthous ulcers ○ Liver: Steatosis ○ Biliary tract: Gallstones , sclerosing cholangitis ○ Joints: Spondylitis, sacroiliitis, peripheral arthritis ○ Circulation: Phlebitis ● Evaluation ○ Stool ■ Escherichia coli (E. coli), C. diff, parasites, fecal calprotectin (85-93% sensitive) ○ Labs ■ CBC ● Anemia ■ Sed rate, CRP - may be elevated ■ Electrolytes, magnesium, albumin, renal and liver tests, iron ○ Sigmoidoscopy or colonoscopy ■ Symmetric, continuous alterations in the mucosal & submucosal layers ■ Biopsy to confirm dx ● Management ○ Goal: Achieve & maintain remission, improve QOL & reduce complications ○ GI referral ■ Determine initial management ○ 5-aminosalicylic acid ( mesalamine ) ■ 1st line to treat mild to mod dz ■ Can come in rectal form if it’s just localized to rectum ○ Oral corticosteroids

■ More severe dz, flare ups ○ Tumor necrosis factor inhibitors (TNF) ■ If unresponsive to initial tx ○ Monitor growth, pubertal changes ○ Nutritional status ■ Watch for nutritional deficiencies ○ Bone health ■ Screen for osteoporosis Celiac Disease ● Overview ○ Autoimmune disorder of the GI tract, triggered by wheat gluten & related proteins in the diet ■ Occurs in pts who are genetically susceptible ■ Frequently co-occurs w/ other autoimmune dzs ■ Affects 1% of the population ○ Gluten be in the American diet ■ We love bread - it’s it wheat, rye, barley, pasta, baked goods ■ Gliadin, which is in gluten is unable in a healthy person to get into the epithelial lining, in pts w/ celiacs, penetrates that lining ○ Immune response that causes a change in the surface of the GI tract, usually small intestine ■ Villi are damaged ■ Pts unable to absorb nutrients well→ vitamin deficiencies ○ Affects all ages, may be asymptomatic ○ Symptoms ■ Constipation, bloating, diarrhea wt loss, nausea ○ Risk factors ■ T1DM, Thyroid disease, IgA deficiency ■ Family history ■ Down syndrome or Turner syndrome @ increased risk ● Exam ○ Skin: Brittle nails, acne or eczema ■ Dermatitis Herpetiformis - cutaneous manifestation ● Rash is very intensely pruritic ● Papules and vesicles develop, excoriation ● On extensor surfaces of elbows & knees ● Can be assoc w/ other autoimmune dzs ex. Fibroiditis ○ Intestinal: Diarrhea, bloating, constipation ○ Mouth: Ulcer & tooth enamel erosion ○ Joint & muscle: pain & swelling ○ Stomach: Pain & nausea ○ In women: infertility, miscarriage, early menopause ○ Lactose intolerance, anemia, dizziness, migraines, depression, low vit D, chronic fatigue ○ In kids: ■ Growth failure or failure to thrive ● Poor linear growth, delayed puberty, amenorrhea

■ Irritable ● Eval & Dx ○ Labs ■ Immunoglobulin A (IgA) antitissue transglutaminase antibody (tTG) if > 2 yo ● Tests may be falsely negative if pt has been avoiding gluten for the past mo ○ Tell them to go eat some pasta for 4 weeks then come back ■ IgA, tTG, and IgA & IgG deamidated gliadin peptides (DGPs) if < 2 years old ■ Iron, folic acid, vit D, vit B12 ■ AST & ALT may be elevated ○ Endoscopy with biopsy to confirm dx if labs are less than 10xs above the upper limits ■ If levels are > 10xs above the upper limits, consider additional testing ex. Endomysial antibody & HLA- DQ w/o endoscopy to dx ● Management ○ Lifelong gluten-free diet ■ Refer to nutritionist ■ No protein from wheat, barley, rye ■ NO beer ○ Meds ■ Oral Dapsone can help speed the resolution ■ Topical steroids to reduce itching ○ Nutrition referral ○ Monitor & treat nutritional deficiencies ○ Monitor growth & development ○ Education ■ Importance of maintaining gluten free diet ■ Even the smallest amount of gluten can trigger symptom return ○ Bone mineral density ■ In older pts ■ Or in kids noncompliant ● Wheat sensitivity ○ Experience abd bloating, diarrhea or constipation ■ May also complain of HA, fatigue ○ Labs are negative ○ Go gluten free and they feel better! Other Malabsorption Syndromes ● Lactose Intolerance ○ Clinical syndrome characterized by ■ Abd pain, N/D, gas, bloating after ingestion of lactose-containing foods ● Cow’s Milk Allergies ○ An antigen-mediated response ○ Peaks in infancy Diverticulosis/Diverticulitis Irritable Bowel Syndrome ● Overview ○ Functional disorder of the bowels ■ Associated w/ abd pain & change in bowel habits ■ Dx requires abd pain for 3 months ■ NO inflammation ○ Population ■ 5-10% of people have it, peaks age 20-39 yo ■ 1.5xs higher in women than men, more common in pts w/ low socioeconomic status ○ Etiology

■ Disturbances in GI motility ■ Mucosal barrier disruption ■ Visceral hypersensitivity ■ Brain-gut dysfunction ● Stress response w/ involvement of neurotransmitters ○ Consultation with a gastroenterologist is indicated for pts w/ a change in bowel habits after age 50; a family hx of celiac dz, colon ca or IBD; evidence of gastrointestinal bleeding; weight loss; fever; nocturnal symptoms; recent antibiotic therapy; or continuing symptoms. ● Symptoms ○ Abdominal discomfort, bloating, distention ○ Abdominal pain related to defecation ○ Altered stool frequency or passage ○ Passage of mucus ○ Triggered by eating ○ Absence of red flags ■ No blood in stool, no wt loss or fever ○ Other ■ Nausea, back ache, fatigue, urinary symptoms ● Rome Criteria ○ Adults ■ Recurrent abdominal pain, on average 1 or more days per week in past 3 months with 2 or more of the following features: ● Related to defecation ● Associated with change in stool frequency ● Associated with change in stool form (appearance) ○ Children: ■ All of following criteria are met for 2 or more months before diagnosis: ● Abdominal pain 4 or more days per month with 1 or more of the following: ○ Related to defecation ○ Associated with change in stool frequency ○ Associated with change in stool form (appearance) ● Dx w/ history, physical & absence of alarm symptoms ○ Exam is usually normal, children are following normal growth curves ○ Considered dx of exclusion ● Bristol Stool ■ Type 1 - separate hard lumps, like nuts hard to pass ■ Type 2 - sausage-shaped but lumpy ■ Type 3 - like a sausage but w/ cracks on its surface ■ Type 4 - like a sausage or snake, smooth & soft ■ Type 5 - soft blobs w/ clear cut edges (passed easily) ■ Type 6 - fluffy pieces w/ ragged edges, mushy stool ■ Type 7 - watery, no solid pieces, entirely liquid ● IBS subtypes ■ w/ predominant constipation ■ w/ predominant diarrhea ■ w/ mixed bowel habits ■ Unclassified: pt who meets dx criteria for IBS but whose bowel habits cannot be accurately categorized into 1 of the 3 subtypes above ● Eval ○ CBC, ESR, CRP, Antibody testing for celiac disease ○ Lactose-free diet ■ If when they go back they get worse, they have a lactose intolerance ○ Stool tests usually not needed unless pt reports a potential exposure to a parasite or foreign travel where they may have been exposed ● Management

○ Establish therapeutic relationship w/ your pt ○ Med interventions (including pharmacotherapy) ■ Abd cramping - try peppermint oil ■ Look for underlying depression or anxiety ● Trial of SSRI ○ Dietary interventions ■ Keep a food journal to see if it’s something they’re eating ■ High fiber diet ● Take cilium such as psyllium or Benefiber ● Helps with diarrhea and constipation ■ Refer to nutritionist if pt interested in FODMAP diet ○ Psychological counseling & psychotherapy ○ Physician consultation & referral to a gastroenterologist are indicated if initial treatment of IBS fails, if organic dz is suspected or found, or if the patient is > 50 years or has an established diagnosis of IBS and is reporting a change in the usual pattern of symptoms. Gastroenterology specialists are also helpful in the comanagement of pts w/ complex IBS. Gastritis ● What is Gastritis? ● Causes ○ H. Pylori ○ Excessive drinking or smoking ○ Prolonged NSAID use Vomiting & Dehydration Vomiting Diff Dx - Age of child helps formulate a list of potential dxs ● Infants ○ Gastroenteritis ○ Gerd ○ Overfeeding ○ Anatomic obstruction: ■ Pyloric stenosis, malrotation w/ intermittent volvulus, intestinal duplication, Hirschsprung dz, antral/duodenal web, foreign body or incarcerated hernia ○ Systemic: ■ Infection, UTI, PNA, hepatitis ○ Pertussis syndrome ○ Otitis media ● Child ○ Gastroenteritis ○ GERD ○ Gastritis ○ Toxic ingestion: Lead, iron or vit A & D ○ Migraine ○ Systemic infection: ■ UTI or pyelo, PNA, Hepatitis ○ Otitis media, sinusitis ○ Appendicitis, small bowel obstruction ○ Meds: ex ipecac, digoxin, theophylline ● Adolescent ○ Gastroenteritis, Gastritis ○ GERD ○ Toxic ingestion ○ Migraine ○ Systemic infection ○ Pertussis syndrome, sinusitis ○ Appendicitis, small bowel obstruction

○ IBD ○ Meds: ex. Ipecac abuse/bulimia ○ Pregnancy, PID ● Clinical findings ○ Hx ■ Symptoms w/ onset, duration, quality, quantity ● Associated symptoms - diarrhea, fever, ear pain, cough ■ Recent exposure to illness, food, injury, stress ■ Past history, family history ■ Meds ■ Mental status/thrist ■ Parental concerns about tearing, urination ○ Physical Exam ■ Growth parameters/vital signs ■ Neuro ■ Abd ■ Resp ■ Assessment of dehydration ● Usually results from infection - primarily viral, causes diarrhea ○ Children @ increased risk ■ Higher body surface area, higher body water content ■ Higher body metabolic rate ■ Decreased ability to communicate thirst ● 4 parameters used for assessment of clinical dehydration are general appearance, eyes (sunken or not), moistness of mucous membranes & presence of tears ● Cap refill, skin turgor & tachypnea considered together are helpful in determining dehydration ○ One of the most useful clinical signs of hydration is cap refill time ○ Management ■ Vomiting ● ID/alleviate cause, rehydration, antiemetics may be used if indicated ■ Dehydration ● Oral rehydration solution for min/moderate ● IV fluids if severe ○ Refer to asynch slides (? what asynch slides I ask myself ? ) ● Initial rehydration, maintenance of fluids, replacement of ongoing losses ● Refeeding should begin as ASAP ● Antiemetics ● Treat fever, monitor urine output ● Refer if toxic, severe projectile vomiting or blood, bile, fecal matter present Constipation in Adults & Children ● Types ○ Adult ■ Primary ● Functional ○ Rome criteria ■ To meet the Rome IV criteria, > 2 must be present for > 3 mos w/ onset 6 mos before dx: ● Fewer than 3 BMs per week ● The passage of hard or lumpy stools (Bristol stool chart types 1 & 2) ● A sensation of straining w/ > 25% of defecations ● A feeling of incomplete evacuation or anorectal obstruction in > 25% of defecations ● Use of manual maneuvers to aid defecation in > 25% of defecations ● Slow transit

○ Prolonged time in btw BMs ○ Assoc w/ abd bloating or discomfort ● Outlet dysfunction ○ Something blocking passage of stool ○ Stricture or prolapse, cancer ● Evacuation disorders ○ Failure to empty rectal contents ● IBS constipation predominant ■ Secondary ● Medications, psychogenic conditions/psych disturbances, neurologic disorders ● Pregnancy, hypothyroidism, hypoparathyroidism, hypercalcemia, DM, hypokalemia, ● LIfestyle ○ Inadequate fiber or fluid intake ○ Ignoring urge to defecate ● Underlying health problems ○ Ex. hypothyroidism, Parkinson’s MS ■ Acute constipation ● Usually occurs w/ dietary changes, travel or stress ● Often resolves on its own or w/ minimal intervention ○ Children ■ Organic ● Hirschsprung disease ○ Esp in infants or newborns who have not passed meconium in the 1st 24 hrs of life ● Celiac ○ Poor waking, vomiting ● Obstruction ● Hypothyroidism ● Spinal cord tumor or mass ● Diabetes mellitus (DM) ● Cystic fibrosis (CF) ■ Functional: ● Dx Criteria ○ Rome IV Criteria for Functional Constipation in Infants and kids must include 2 or more of the following occurring at least 1 per wk for a min of 1 month with insufficient criteria for a dx of IBS: ■ 1. 2 or fewer defecations in the toilet per week in a child of @ least 4 years ■ 2. At least 1 episode of fecal incontinence per week ■ 3. Hx of retentive posturing or excessive volitional stool retention ■ 4. Hx of painful or hard BMs ■ 5. Presence of a large fecal mass in the rectum ■ 6. Hx of large diameter stools that can obstruct the toilet ■ 7. After appropriate evaluation, the s/s cannot be fully explained by another medical condition. ● Encopresis ○ Encopresis = Fecal Incontinence, is most often defined as repetitive, voluntary, or involuntary passage of stool in the underwear or inappropriate places after an age when the child should be able to control BMs, usually 4 years old. ● Eval ○ True clinical dx of constipation is finding of a large amount of feces in the rectal ampulla on digital exam or excessive feces in the colon, rectum or both on abd xray ■ If accompanied by N/V, fever & abd pain it may indicate an ileus or ischemia → send to ED!!! ○ History ■ Alarm symptoms ■ Family history

● Colon ca, IBD ■ Medications ● Anticholinergics, diuretics, iron can lead to constipation ■ Diet and lifestyle ● Sedentary, dehydrated ● Toddlers often drink too much milk, not enough milk, can lead to constipation ○ Exam ■ Kids ● Growth & development ● Hard stool ■ Abd exam ● Look for distension, mass, hard stools ● Rectal exam for signs of stricture or prolapse ○ If pt is > 50 yo or alarm symptoms ■ Fecal occult blood test (FOBT) ■ Radiography ■ Colonoscopy ○ If pt is > 50 yo or suspected 2ndary cause ■ CBC, lytes, Ca, blood sugar, Thyroid function tests, UA ○ Children ■ If no improvement with treatment or suspect organic constipation ● Celiac panel ● Thyroid stimulating hormone (TSH) ● Calcium ● Glucose ■ Kidney, ureter, and bladder (KUB) ● If you suspect impaction ● Atypical presentation or diagnosis unclear ○ May need GI referral ● Management ○ Hydration ○ Veggies, increase fiber ■ 25-50 g of fiber a day ■ Prunes are helpful ○ Exercise ○ Meds ■ 1st line polyethylene glycol ● May take 2-3 days to produce BM ● Few side effects ■ Bulk forming or osmotic laxatives, stool softeners ● Bulk forming - Metamucil ● Stool softeners - Docusate sodium ● Osmotic - Miralax, Milk of Mag ■ Impaction? ● Oral stimulant laxatives ex. Senna, Dulcolax ● Adults can get suppository laxatives

GI Tract Tumors ● Esophageal Carcinoma ○ Risk factors: Smoking, alcohol use, obesity ○ Clinical Presentation: Dysphagia & weight loss ○ Dx: CBC, CMP, EGD w/ biopsy ● Gastric Cancer ○ Risk factor: H. pylori is primary risk factor ○ Clinical Presentation: Unexplained weight loss, upper abd pain, anorexia, nausea, early satiety ○ Dx: CBC, LFT, stool occult, EGD ● Small bowel Cancer ○ Average age 50-70 yo w/ male predominance ○ Increased risk of small bowel cancer in pts w/ Crohn disease ○ Abd pain is the most common symptom ○ Imaging: small bowel follow-through, CT scan Colon Cancer ● Overview ○ 2rd leading cause of death in the US ○ Majority of colon ca are adenomas ■ located in the rectum ⅓ ■ located in the colon ⅔ ● Risk Factors ○ Age > 50 yo ○ Prior colorectal ca, IBD ex. Ulcerative colitis ○ Family hx ■ Hereditary & genetic factors ■ Familial polyposis syndromes ○ Smoking, high fat high caloric diet ○ Familial polyposis syndromes ● Patho ○ Develop from adenomatous polyps or hyperplastic ○ Arise from adenomatous polyps ○ Progress into stage 1, become more noduler

○ Stage 2 ○ Stage 3 - metastasized into regional lymph nodes, grows in size ■ Can metastasis to lungs, liver, etc ● S/S ○ Depends on location of tumor ○ Often asymptomatic ○ Wt loss, blood stools, anemia ○ Decreased caliber in stool ○ Sudden onset of change in bowel habits and/or appearance ■ Ex. sudden onset of constipation or diarrhea ○ Gas pain, abd pain ○ More advanced ca → pt presents w/ abd pain or palpable mass ● Tests → Colonoscopy w/ biopsy ● Refer to GI, oncology, surgery for tx ○ Usually have surgery and treated w/ chemo Evaluation of Elevated Liver Enzymes ● Overview ○ Liver transaminase - AST & ALT ○ Mild elevation = less than 5 xs upper limits of normal ■ > 5 xs, evaluated differently ○ 10% of the pop have asymptomatic elevation of liver transaminase ■ < 5% have serious underlying dz ● What’s wrong with elevated LFTs? ○ ALT and AST respond to hepatocellular damage ■ ALT more specific to the liver ■ AST elevated in extrahepatic causes ● Ex. thyroid disorder, celiac, muscle disorder ■ Alcoholic liver dz ● AST to ALT ratio is usually > 2 ● Common causes of elevated LFTs ○ Before starting to investigate repeat lab work in a few weeks ○ Nonalcoholic fatty liver disease (NAFLD) ■ 25-50% of cases ○ Nonalcoholic steatohepatitis ○ Alcoholic liver disease ■ Sometimes overlap w/ NAFLD ○ Medications ■ OTC meds - NSAIDS, Tylenol ■ Certain antibx, antipsychotics ○ Infection ■ Hep B and Hep C ● Check Hep B surface antigen and hep C antibodies ○ Hereditary Hemochromatosis ■ Autosomal recessive genetic dz ■ Increased absorption of iron in the intestinal tract ● Check serum iron, TIBC, Ferritin ○ If ferritin is > 250 in men or 300 in women, check for hemochromatosis gene ○ Alpha-1 Antitrypsin deficiency ■ Cause of COPD, genetic disorder, also assoc w/ liver dz ○ Autoimmune Hepatitis ■ More common in young women ■ Assess w/ serum protein electrophoresis & IgG ○ Wilson dz ■ Genetic, ineffective copper metabolism ■ Copper can build up

■ Can cause neuropsych problems or symptoms ■ Evaluated w/ serum ceruloplasmin ■ More common in pts < 35 yo ○ IBD ○ Hemolysis ● Work up ○ Based off of H&P ■ Look if they have metabolic syndrome, risk factors for fatty liver disease ○ Labs ■ Lipid panel, A1C, Hep B & C ■ Iron levels - serum iron, TIBC, ferritin ■ CBC, albumin ○ If labs inconclusive - consider checking for more rare disorders & Abd US Nonalcoholic Fatty Liver Disease (NAFLD) ● Overview ○ 20% of americans have fatty liver dz ○ Most pts have DM, usually T2 ○ 7% of kids w/ fatty liver dz ○ Associated w/ increased BMI & obesity , certain meds ○ Steatosis w/o hepatic cell injury ■ Inflammation of the liver can cause fibrosis to develop, risk of progressing to cirrhosis, higher risk of developing hepatocellular ca ● Risk Factors ○ Obesity, metabolic syndrome, insulin resistance, PCOS ○ Elevated TG, increase in waist circumference ○ Severe wt loss ● Risk factors for progression of dz ○ HTN, DM, increasing insulin resistance & weight gain ● Symptoms ○ Often asymptomatic ■ Incidental elevation of AST & ALT or may be found on an imaging study ○ Fatigue ○ Right upper quadrant abdominal fullness or pain ○ Muscle weakness ○ Jaundice occurs late and indicates advanced liver disease ○ Abdominal obesity, possibly hepatomegaly on exam ● Dx of NAFLD ○ Hepatic steatosis on imaging or histology ■ Biopsy is not needed for diagnosis ○ No significant alcohol consumption ○ No other etiologies ○ Abnormal liver chemistry ■ Aspartate aminotransferase (AST)/ alanine aminotransferase (ALT): normal to 1-4 times upper limit ■ AST/ALT ratio less than 1 ■ Ruled out other causes of LFT elevation ○ Alkaline phosphatase may be 2xs upper limit ○ Bilirubin, prothrombin time (PT), albumin are normal ■ Elevated bili later in dz process ■ Cirrhosis abnormal PT, albumin low ○ Liver biopsy needed to diagnosed steatohepatitis ■ This is when fatty liver progresses to hepatitis, there’s fibrosis ● Management ○ Weight loss ○ Hypocaloric diet, avoid processed food, fructose

■ Mediterranean diet ○ Exercise ○ Avoid excessive alcohol ■ Really shouldn’t drink any alcohol ○ Monitor liver enzymes ■ Q 6-12 mo ○ Screen for DM ○ Statins if they have HLD Cirrhosis ● What is it? ○ End stage consequence of liver fibrosis ■ Most common cause of cirrhosis is either Hep C or Hep B, alcoholic liver dz, NASH & NAFLD ○ Normal liver tissue is replaced w/ scar tissue ■ Leads to development of nodules on the liver ■ Impair liver function ■ Necrosis w/ liver damage & fat deposits on the liver ○ Once cirrhosis occurs, it is not reversible ● S/S ○ Nonspecific symptoms of anorexia, weight loss, weakness, fatigue or signs and symptoms of hepatic decompensation including jaundice, pruritus, signs of upper gastrointestinal bleeding, abdominal distension from ascites, and confusion due to hepatic encephalopathy ● Exam: ○ Jaundice, spider angiomas ○ Gynecomastia, ascites, splenomegaly, palmar erythema, digital clubbing, and asterixis. ○ ● Complications ○ Increased risk of hepatocellular ca ○ Portal HTN ○ Asymptomatic, insidious onset ○ Pruritus, fatigue, weakness, dark urine, pale stool ○ Jaundice, spider angiomas, palmar erythema ○ Gynecomastia ○ Nausea, vomiting, neuropsych issues ■ Hepatic encephalopathy ○ Scarring & fibrosis → portal HTN ■ Development of ascites and esophageal varices ● Labs ○ ALT & AST may be normal or elevated ○ Elevated serum bilirubin ○ Elevated alkaline phosphatase/gamma-glutamyl transpeptidase (GGT) ○ PT & INR elevated in advanced dz ○ Hyponatremia, Low albumin ○ Abnormalities in the CBC ■ Anemia, thrombocytopenia, pancytopenia ● Imaging ○ US/CT/MRI → liver appears shrunken, irregular & nodular ● Work Up /Dx ○ Usually made by clinical, lab & imaging studies ■ May get liver biopsy ○ Find out underlying cause ■ Alcoholism, Hep C, fatty liver dz ● Management ○ W/ liver specialist ○ Slowing or reversing the progression of liver disease by treating underlying causes ○ Preventing superimposed insults to the liver by vaccinations & avoiding hepatotoxins

○ ID meds that require dose adjustments or should be avoided entirely ■ Monitor for complications, side effects of certain treatments ○ Preventing, ID, & treating the complications of cirrhosis ■ Managing symptoms (muscle cramps) & lab abnormalities (hyponatremia, thrombocytopenia, elevated INR) ○ Determining the appropriateness & optimal timing for liver transplantation ○ Promote healthy lifestyle ■ Diet, exercise ○ Support and education for family Cholelithiasis ● What is Cholelithiasis? ○ ● Symptoms ○ RUQ or epigastric pain, often colicky & post prandial ○ Pain may radiate to shoulder ○ N/V may be present ● Cholecystitis ○ Same as cholelitiasis +: ■ Murphy’s sign present ■ Fever & chills may be present ● Cholangitis ○ Same as cholecystitis ○ Jaundice ○ AMS, shock Gastroesophageal Reflux (GER) & Gastroesophageal Reflux Disease (GERD) in Infants ● Overview of GER ○ Retrograde movement of gastric contents from stomach to the esophagus ○ Very common, occurs in 40-70% of infants ○ Postprandial reflux regurgitation w/ o w/o vomiting, relaxation in the lower esophageal sphincter, stomach contents will reflux up ■ Also due to increased intraabdominal pressure that exceeds pressure in the sphincter causing infants to regurgitate w/ occasional vomiting ○ Can occur multiple times a day ○ Recurrent regurgitation w/ or w/o vomiting ■ “Happy spitters” → can occur up to age 18 mo ● Decreases 6-12 mo, LES weakness ■ Does not cause them to cry or arch their back, gaining weight appropriately ● GERD w/ complications - happens in about 1.5/100,000 starting @ 1 wk old, before 6 mo ○ Recurrent regurgitation with or without vomiting ○ Feeding difficulties/refusal ○ Irritability and excessive crying ○ Back arching ○ Cough or recurrent stridor or wheezing ○ Hoarseness ○ Poor weight gain ○ Sleep disturbances ● Differentials ○ Colic, cow’s milk allergy, hiatal hernia ● Red Flags - send urgently to ped GI provider ○ Onset after six months ○ Neurological signs ○ Bilious or projectile vomiting ■ Think pyloric stenosis

○ Bloody emesis, Bloody stool ○ Nocturnal vomiting ○ Abdominal distention ○ Diarrhea or constipation ○ Lethargy ● Dx ○ Based on H&P ■ Absence of red flags, pt is thriving ■ Hx ● Heartburn, acidic regurgitation ■ Physical ● Review Ht, wt, head circumference ● Signs of FTT ● Torticollis - neck arching ● Hoarseness, tooth erosion ● Anemia ● Rash, recurrent diarrhea, persistent/early morning vomiting ○ Dx in the setting of chronic symptom distress w/ or w/o mucosal damage ● Diff Dx ○ Cholelithiasis, PUD, gastritis, angina, esophageal motility disturbances, & GI malignant neoplasms ○ Cardiac ischemia, aspiration PNA, gastric obstructing tumor, pyloric stenosis ○ Peptic stricture, Barrett’s esophagus ○ Zollinger-Ellison syndrome, achalasia ● Tx ○ GER - Treated conservatively ■ Avoid large feeds, more small frequent feedings ■ If infant is breastfeeding, have mom avoid dairy as it can sometimes make it worse ■ If infant is formula fed - can be switched to hypoallergenic formula ■ Do not lie child down supin immediately after feeds ■ Consider thickeners ■ Typically improves by 6 mo, resolves by 12-18 mo ● If not better by 18 mo → refer to GI! ○ GERD ■ Lifestyle modifications ● Hydrolyzed formula, mom changes diet, small frequent feeds for the first 2-4 weeks ● Positioning- unlike older kids & adults, upright positioning in infants can actually worsen reflux ■ If infant fails lifestyle mods ● Trial of acid reducer like a PPI or H2 blocker for 4 weeks ○ PPI - shorter course 1-2 wks ● If the infant gets better, continue for a period of time ■ Follow up to determine what their response is 1st to the conservative tx, and @ least 3-4 weeks after starting PPI ● If not getting better → refer to GI ● Monitor weight gain and symptoms GERD in Adults ● Overview ○ Most common GI related dx in primary care ○ 18-27% of people in the US have it ○ Reflux of stomach contents into the esophagus causes troublesome symptoms or complications. Relaxation of the lower esophageal sphincter and in conjunction w/ that, increased intraabdominal pressure ○ Prompt medical evaluation by a gastroenterologist is indicated if the patient has unintentional weight loss, dysphagia for solids or liquids, odynophagia, unexplained anemia, or chronic tobacco and alcohol exposure. ○ Alarm symptoms include GI bleed. anemia, dysphagia, odynophagia, unintentional weight loss, early satiety, age > 55 at presentation, recurrent vomiting, and epigastric mass. ● Risk Factors

○ Obesity ○ Pregnancy ○ Tight clothes ○ Hiatal hernia ○ Smoking, alcohol, fat, & coffee ○ Gastric and esophageal dysmotility ■ Ex. scleroderma, neuropathy ○ Large meals ○ Medications ■ Anticholinergics, nitrates, Ca channel blockers ● Symptoms ○ Typical ■ Heartburn → Discomfort or burning behind the sternum, may radiate to neck or throat ■ Worse after eating and lying supine ■ Better after antacids ■ Regurgitation of stomach contents into mouth or hypopharynx ■ Eldery pts more likely to have anorexia, wt loss, anemia ○ Atypical ■ Epigastric fullness, epigastric pressure, epigastric pain, ■ Dyspepsia, nausea, bloating, & belching ■ **Atypical symptoms do not respond well to PPI tx** ○ Extraesophageal ■ Chronic cough, wheezing, asthma, bronchospasm, SOB ● Add burning of mouth & tongue ■ Globus sensation ● Feeling like something is kind of stuck in the throat ■ Dental erosions ■ Hoarseness, laryngitis ■ Sore throat or burning throat, dysphagia ■ Postnasal drip ■ Throat clearing ■ Asthma/wheezing ● GERD can also exacerbate asthma ● Exam ○ Often normal ● Dx ○ Made on history, physical & response to treatment ■ Testing not indicated ○ Differentials ■ Functional dyspepsia ■ Coronary artery disease (CAD) ● Since it can cause substernal chest pain ■ Esophageal spasms ■ Peptic ulcer disease (PUD) ■ Gastric cancer ■ Gallbladder disease ● Can cause pain in the epigastric area or in the chest ○ Dx Testing should be considered in pts w/ ■ A failed empirical trial (4-8 wks of twice daily PPI) suggesting an alternative dx ■ W/ sudden onset of symptoms in a patient > 50 yO ■ W/ alarm symptoms suggesting complicated dz (anemia, dysphagia, bleeding, odynophagia), ■ W/ long-standing symptoms of sufficient duration to put pts @ risk for Barrett’s esophagus ■ Additional testing: CBC, H. pylori testing, ambulatory pH testing, gastric emptying scans ○ Nonerosive Reflux Disease ■ No mucosal changes noted on EGD

● Reflux hypersensitivity - symptoms correlate w/ physiologic reflux ● Functional heartburn - symptoms do not correlate w/ physiologic reflux ○ Erosive Reflux Disease ■ Inflammatory changes noted on EGD ● Management ○ Lifestyle changes ■ Quit smoking, exercise regularly, sit up straight ■ Eat small meals throughout the day, chew food slowly ● Avoid food right before bedtime ○ Don't eat food & then go to bed ○ Allow 3 hours in between dinner and bedtime ■ Avoid heartburn triggers ● Less fatty food, spicy foods & alcohol ● More whole grains and fibers ■ Wear loose & comfortable clothing ■ Sleep w/ your head & shoulders propped up ■ Minimize caffeine & alcohol consumption ■ Avoid lying down for @ least 3 hrs after a meal ○ Meds ■ PPI for 8 wks ● First choice in controlling symptoms, healing esophagitis & improving QOL ● Recommended for maintenance @ lowest dose ○ Can increase to 2xs daily ○ Second dose should be given 1 hr before evening meal ● Take 30-60 min before a meal ● Monitor for vit B12, can interfere w/ absorption of calcium, increase risk of c. diff ■ H2 blocker ex. Cimetidine or famotidine ● Can be used for maintenance w/o esophagitis ■ Antacids ● As needed if someone’s having breakthrough symptoms ○ Endoscopy ■ Not needed for monitoring dz ■ Consider if someone has alarm symptoms - wt loss, anemia or dysplasia especially in older patients

● Complications ○ Esophagitis ■ Inflammation in the esophagus and can cause ulcerations ○ Stricture ○ Barrett esophagus ■ Small % develop into esophageal adenocarcinoma ○ Adenocarcinoma (rare) ○ Asthma ■ Trigger more wheezing ○ Tooth erosions ● Alarm symptoms!! ○ GI bleed, anemia ○ Dysphagia, odynophagia ○ Unintentional wt loss, early satiety ○ Age > 55 @ presentation ○ Recurrent vomiting, epigastric mass Barrett’s Esophagus ● Overview ○ Metaplastic change ■ Change in the distal esophagus to columnar epithelial cells ○ Normal esophagus ■ Squamous cell, squamous epithelial tissue line esophagus ○ Most often occurs in response to reflux of gastric contents refluxing up into the esophagus ■ Can progress to adenocarcinoma ● Only 0.12% of cases ■ If pt has high grade dysplasia those pts are at higher risk of developing cancer ● Risk factors ○ Chronic GERD, smoking ○ Males over the age of 50 yo ○ Hiatal hernia & obesity ● Screening ○ NO routine screening ○ Only screen pts w/ GERD who have alarm symptoms or red flags ○ Pts w/ multiple risk factors ● Tx in Barrett’s ○ No dysplasia? Upper endoscopy Q 3-5 years ○ Low grade dysplasia? Endoscopy every 6-12 months ○ High grade dysplasia? Treat! ○ Consult w/ GI ■ Treat underlying GERD w/ PPI Appendicitis ● What is it? ○ Inflammation of appendix leading to necrosis, perforation, peritonitis, abscess ○ Average age 6-10 yo; perforation more common in kids < 5 yo ● Clinical findings ○ Hx ■ Sequence of symptoms ← Most reliable info gained ■ Pain shifting to RLQ; nausea/vomiting after pain ● Pain is initially poorly defined periumbilical pain (earliest sign) then a shifting of pain to the RLQ may occur after a few hours and becomes more intense, continuous, and localized. ■ Anorexia in 50% of children ■ Stool low volume with mucus ■ Fever neither sensitive nor specific

■ Scoring system useful ■ Perforation leads to lessening of symptoms ○ Physical ■ Involuntary guarding, RLQ rebound tenderness; maximal pain at McBurney point ■ Heel-drop jarring test ■ Positive Psoas sign, Rovsing sign ■ Tenderness, possible mass w/ rectal exam ● Dx ○ CBC with differential ○ Amylase, lipase, liver enzymes to rule out other causes ○ UA, stool examination ○ US – enlargement of appendix; CT has highest accuracy ○ B-hCG to rule out pregnancy ● Diff Dx ○ Gastroenteritis - vomiting precedes pain, stool is high volume & watery ○ Constipation, UTI, pregnancy, PID, intestinal obstruction, peritonitis, intussusception ● Management ○ Surgical consultation for appendectomy ○ Open or laparoscopic appendectomy if non-perforated ○ Follow-up 2-4 weeks postoperatively ● Complications ○ Perforation, peritonitis, abscess, ileus, obstruction, sepsis, shock, death Intussusception ● What is it? ○ Invagination of bowel into colon, usually @ ileocecal valve ○ 80% before age 2 ○ Most frequent cause of intestinal obstruction in kids ● Clinical findings ○ Hx ■ Classic triad: Intermittent colicky pain, vomiting, bloody mucous stools (currant jelly) ■ History of URI common ■ Lethargy common ■ Fever usually late sign of infarction/gangrene ○ Physical ■ Glassy-eyed, groggy between episodes ■ Dance sign: Sausage-like mass in RUQ ■ Distension, tenderness of abdomen ■ Grossly bloody or guaiac-positive stools ○ Dx ■ Abdominal flat-plate radiograph may appear normal ■ Abdominal US very accurate ■ Air contrast enema both diagnostic and treatment modality ○ Diff Dx ■ Incarcerated hernia, testicular torsion, acute gastroenteritis, appendicitis, colic, & intestinal obstruction ○ Management ■ ER w/ pediatric radiologist & surgeon ○ Complications ■ Swelling, hemorrhage, incarceration & necrosis of the bowel requiring bowel resection may occur Anal Fissure ● What is it? ○ Small tears in anal mucosa ○ Passage of frequent or hard stools usual cause ○ Most common cause of rectal bleeding in peds ● Hx

○ Crying with bowel movement ○ Bright red streaks of blood ○ Withholding of stool ● Diff dx ○ Other sources of lower intestinal hemorrhage ● Management ○ Treat cause ○ Local wound care ■ Sitz baths, hydrocortisone cream, KY jelly ● Complications - recurrence common ● Education ○ Avoid constipation, encourage regular toilet habits, avoid laxatives