Step up to Medicine Stable Angina- fixed atherosclerotic lesions narrowing coronaries.

Occurs when demand exceeds supply o Risk Factors: DM, HTN, HLD, Cigs, Age (M>45, F>55), FHx, high Homocysteine o Prognosis EF< 50% has increased mortality Worst Vessel- Left Main, then twothree vessel disease o Clinical- squeezing chest pain <15 mins brought on by exertion and relieved by rest or nitroglycerine o Dx- Resting EKG is NORMAL in STABLE- if Q waves, then prior MI, if ST/T changes then UNSTABLE angina. If the EKG is NORMAL then see if the patient can exercise If they can, they should have an exercise stress EKG o IF THIS IS +, MUST DO CATH!!! o + means ST depression (subendocardial), heart failure, or arrhythmia. Can also do a Stress ECHO which is more sensitivie and can diagnose valvular disease. o IF THIS IS +, MUST DO CATH!! o Look for wall motion abnormalities before and after exercise During this you can inject thallium and see if all of the heart is perfused with the thallium. IF YOU DO THIS, must see if the area is REVERSIBLY ischemic as the patient stops exercising because you can do PTCA or CABG to revasculairze these areas. If patient canNOT exercise: Pharmacologic Stress Test: IV Adenosine, dipyridamole or dobutamine Holter Monitoring if concerned for silent ischemia Coronary Cath with Angiography- sees diameter of coronaries and, if >70%, then can refer for CABG. o Treatment- Lifestyle changes (see risk factors), ASA (decreases risk of MI, indicated in ALL pts with CAD), Beta-Blockers (decreases cardiac work) Nitrates reduce preload by being a generalized vasodilator and is mainly a symptomatic tx. CCB cause coronary vasodilation and afterload reduction- 2ndary tx to nitrates and Beta Blockers ACEIs/Diuretics IF CHF IS ALSO PRESENT Revascularization- does NOT result in reduced incidence of MI, but DOES reduce symptoms Based on Limitations and Overall Risk: Mild Disease- Normal EF, mild angina or single vessel o Nitrates and beta blockers or CCBs Moderate Disease- Consider angio for PCTA or CABG Severe Disease- 3 vessel disease, decreased EF or SEVERE angina) o Coronary Angiography and consider CABG Indications for Cardiac Cath:

Positive Stress Test Angina + Noninvasive tests are nondiagnostic Persistent despite optimal medical therapy Occurs after recent MI o Severely symptomatic with urgent diagnosis needed o Evaluation of valvular diseaseo STEMI Indications for PTCA: one or two vessel disease for proximal lesions. o Up to 40% can re-stenose after 6 months, but will not re-stenose usually if you are clear up until 6 months. This rate is reduced by stenting. o Also an alternative to thrombolytic therapy during MI if thrombolytic tx is contraindicated. CABGo Indicated in left main, three vessel dz, LAD + one other vessel or SEVERE ischemia Unstable Angina Pectoris: Steps: Get cardiac enzymes and EKGGive ASAGive Heparin o Oxygen DEMAND IS UNCHANGED, but SUPPLY is decreasedreduced coronary flow. o Stenosis that has enlarged (thrombus, hemorrhage or plaque rupture) Patient who has chronic stable angina that is now increasing in duration, frequency or intensity. New-onset angina that is SEVERE and WORSENING Angina at rest o Diagnosis-same as stable angina though must stabilize with medical management before stress test Exclude MI o Treatment- Admit to tele, get IV access and give O2. Pain control- nitrates and morphine ASA, Beta Blockers (first line if no contraindications) LMWH or Heparin 2 days at least with PTT 2-2.5x normal Abciximab- IIb/IIIa inhibitors especially if stenting/PCTA will occur Most do not require cath- 90% respond to medical tx If they respond to medical treatmentStress EKG to assess need for revascularization Cath if there is no response to medical therapy Long term Tx Continue ASA, Beta Blockers, Nitrates, start statins Treat diabetes, HTN, smoking cessation Folate controversial for homocysteinemia. TIMI Score-Age>65, More than 3 risk factors, Known CAD (>50% stenosis), ASA use in last 7 days, Elevated Cardiac Enzymes, 2 episodes of angina in last 24 hours, ST changes Variant Angina (Prinzmetals Angina) o Transient coronary vasospasm which many times has a fixed atherosclerotic lesion.

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Occurs AT REST. Usually associated with a VENTIRCULAR ARRHYTHMIA ST-Elevation on EKG during chest pain (TRANSMURAL ischemia) Diagnosis- Coronary Angiography with ergonovine which should provoke the vasospasm. o Treatment- Vasodilators (Ca Channel Blockers and nitrates) Myocardial Infarction- necrosis of myocardium due to interruption of blood supply. Most cases due to atheromatous plaque rupturing into lumen with thrombus forming on top of lesion. 30% mortality rate with 50% of those being PRE HOSPITAL. o Clinical Features Substernal, crushing chest pain with radiation to jaw, back, arms, neck on left. Usually lasts longer than 30 minutes Asymptomatic in 1/3. Most common asymptomatic pts are postop, elderly, diabetic and women. Dyspnea, Diaphoresis, Weakness, N/V, Syncope Sudden cardiac death usually due to VFib o Diagnosis EKG shows Peaked T waves VERY early which are usually missed. Then shows ST Segment elevation (transmural injury), then shows Q waves which are specific for necrosis and show up late. T wave inversion is sensitive but not specific. ST depression is indicative of subendocardial injury. Enzymes CKMB is gold standard- 4-8 hrs48-72 hrs. Measure q8h x 24h Troponin T and I- 3-5 hrs5-14 days. Greater specificity. 18h for 24 hrs o Falsely elevated in patients with renal failure Thrombolytic Therapy- should happen within 6 hours but is OK up to 24 o Indications include STEMI refractory to nitroglycerine. tPA is first choice o Contraindications- >180/110 BP, Trauma, PUD, Stroke, Invasive Procedure, Aortic Dissection Diagnosis of MI: Treatment of MIo Tele, IV access, supplemental O2 and analgesics (nitrates, morphine) o ASA, Beta Blockers, ACEIs, Statins- all long term medications that should be started o Oxygen can help to limit myocardial injury o Nitrates decrease preload (demand) and decrease afterload. Dilate coronary arteries also (increases supply) o Morphine- for analgesia o Heparin- LMWH is better Complications of Acute MIo Pump Failure- Most common cause of in-hospital mortality and can be treated medically if mild with ACEI and diuretic. If severe, could cause cardiogenic shock, requiring invasive monitoring o Arrhythmias PVC- conservative tx- no antiarrhythmics AFib- usual A fib tx

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VTach- if sustained, requires tx. Hemodynamically unstable pts need CARDIOVERSION, and stable pts need antiarrhythmic tx with IV amio VFib- defibrillation immediately Paroxysmal SVT Sinus Tachy- can be caused by pain, fever, stress etc and can worsen ischemia. TREAT THE UNDERLYING CAUSE Sinus Brady- common in EARLY MI. Protects against myocardial demand. If severe or pt is unstable, give atropine. Otherwise, no tx Asystole- Defib immediately. HIGH mortality. Should establish transcutaneous pacing. AV Block- ischemia in the conduction tracts. 1st degree and 2nd degree Type I req no tx 2nd degree type II and complete assoc with anterior wall MI. Place a pacemaker. Could be indicative of inferior MI also, which has better prognosis than the former and IV atropine may be used initially. o Recurrent Infarction- short term and long term mortality increased by either extention of the CURRENT infarction OR a new area infarcted. Dx by REPEAT ST segment elevations within first 24 hrs. Tx- Repeat thrombolysis or PTCA or cath. o Rupture of Free Wall- usually fatal and happens during first 2 wks after MI with 90% mortality rate due to hemopericardium and cardiac tamponade. Tx is pericardiocentesis and surgery. o Rupture of IV Septum- within 10 days of MI. Higher rate of chance of successful therapy than free wall rupture. Tx= surgery emergently o Papillary muscle rupture- Mitral regurg. Get an IMMEDIATE echo if suspectedtx= emergent surgery + Nitroprusside for afterload reduction o Ventricular Pseudoaneurysm- incomplete free wall rupture contained by pericardium. Do a bedside echo. SURGICAL EMERGENCYcan become free wall rupture o Ventricular ANEURYSM- RARELY ruptures but commonly causes VTach. Manage Medically o Acute Pericarditis- ASA is treatment with NSAIDS CONTRAINDICATED (inhibit scar formation in heart) o Dresslers Syndrome- weeks to months after MIimmunologic rxn w/ fever, malaise, pericarditis, leukocytosis and pleuritis. Treat with ASA DDx of Chest Pain: o Heart- Angina, MI, Pericarditis, Aortic Dissection o Pulmonary: PE, pneumothorax, pleuritis, pneumonia, asthma o GI- GERD, Esophageal spasm, PUD, rupture of esophagus o Chest Wall- costochondritis, muscle strain, rib fracture, herpes zoster o Psychiatric- panic/anxiety attacks CHF- an inability of the heart to meet the bodys circulatory demands o SHOULD DO: CXR for pulm edema, caediomegaly EKG Enzymes to ROMI CBC (anemia)

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Echo (EF, pericardial effusion) Frank Starling Relationship- increasing preload leads to greater contractility. If preload is low there is no diff in performance between normal and failing heart but with a failing heart, there is less contractility leading to heart failure symptoms. High Output Heart Failure- INCREASE in ouput needed for requirements of peripheral tissues to be met Anemia, Pregnancy, Hyperthyroid, AV Fistula, Pagets Dz of bone, Mitral Regurg, Aortic Regurg Systolic Failure- impaired contractility leading to low EF. Causes include recent MI, CM, or myocarditis. Diastolic Failure- either due to stiffness of ventricle or due to impaired relaxation (shown on Echo) Due to HTNsive heart dzLVH (stiff wall) Due to Aortic/Mitral stenosis or aortic Regurg Due to Restrictive CM (amyloid, sarcoid or hemochromatosis) Clinical Features: Dyspnea, Orthopnea, PND, Nocturnal cough, Confusion/Memory Impairment (inadequate brain perfusion), Diaphoresis at rest Signs of LV failure: Displaced PMI to left (cardiomegaly) Pathologic S3 (heard best at apex) S4 (left sternal border)- atral systole into noncompliant ventricle. Crackles/Rales- signifies at least moderate LV failure Dullness to lung percussion at bases (fluid in alveoli) Signs of RV Failure: Pitting edema Nocturia (increased venous return with elevation of legs) JVD/HJR Ascites NYHA Classes of HF: Symptoms: I- only with vigorous activity do you get symptoms Restrict sodium and start furosemide for pulm congestion ACEI as first line II- prolonged or moderate exertion Loop Diuretic and ACEI Add a beta blocker III- usual activities of daily living IV- at rest Add digoxin to loop and ACEI (but does NOT improve mortality) Spironolactone if STILL symptomatic after all this Diagnosis: CXR shows Kerley B Lines (short horizontal lines near periphery of lung) and interstitial markings along with possible pleural effusion

Echo-INITIAL TEST OF CHOICE- helps determine if due to pericardium, myocardium or valvular problems. Also estimates EF (<40%= systolic dysfxn) EKGnonspecific but can show hypertrophy or enlargement MUGA Scan- RBCs tagged with technetium 99 and imaged during stress. Gives precise WMAs and EFs. Cardiac Cath- quantitative info about diastolic vs systolic. Consider coronary angiography to R/O CAD as cause for CHF Stress Testing- to identify ischemia and differentiate pulm vs cardiac o Treatment: Systolic Dysfxn- Sodium restriction, most diuretics do NOT improve mortality or prognosis Spironolactone was shown in the RALES trial to improve mortality in CLASS III or IV in the long term. Other diuretics are only for symptomatic relief ACEIs- venous and arterial dilation leading to decreased preload and afterload. Prolong survival in combination with diuretic. o ALL pts (even asymptomatic) w/ CHF should be on ACEI but start at low dose to prevent hypoTN. o MUST MONITOR BUN, BP, K, Cr ARBs- if unable to tolerate ACEIs B-Blockers (ESP CARVEDILOL)- PROVEN to decrease mortality if POST MI. o Slows down tissue remodeling and thus slows down progression of heart failure. DIgoxin- Positive inotrope- in ppl <30% EF but does NOT show mortality benefit. Can be added to diuretic and ACEI in SEVERE CHF o Toxicity- N/V anorexia, AV block, A Fib, Green vision, Disorientation Hydralazine/nitrates- if do not tolerate ACEIs Diastolic- symptomatic tx. Premature Atrial Complexeso Early beat in atria which can be due to excess adrenergic stim, drugs, alcohol, tobacco, ischemia, electrolytes, infection o Early P waves that look different than normal and normal QRS. Can cause palpitations or give rise to Paroxysmal SVTs. o Usually require no tx but if symptomatic (ie palps) can get beta blockers. PVCs- early beat from focus originating in ventriclespreads to other ventricle o Causes- hypoxia, electrolyte abnormalities, stimulants, caffeine, meds o SLOWER than normal conduction and therefore, WIDE QRS o Most are asymptomatic but if the patient is symptomatic, beta blockers can be used. o If frequent and repetitive, can be at risk for sudden cardiac death due to VFib. SHOULD ORDER an EP study for evaluation for an ICD or cryoablation. Tachyarrhythmias-

Afib- Chaotic, rapid pattern with irregular, rapid ventricular rate. Atria quiver continuously with a rate over 400 bpm which is transmitted to the ventricles through an AV node which only allows 75-175 of these beats through. Many causes including MI, CAD, HTN, pericarditis, PE/pulmonary, Thyroid dysfxn (hypo/hyper), Sepsis or other systemic illness, Stress, Alcohol, Sick Sinus Syndrome, Pheo Clinical Features- fatigue, exertional dyspnea, palps, dizziness, angina, syncope, irregularly irregular pulse, BLOOD STASIS If patient is hemodynamically stablerate control to 60-100 bpm with CCB (first line) or beta blockers (2nd), or dig/amio (3rd). If the duration of Afib <48 hrscardiovert immediately while starting pt on IV heparin (still require 4 weeks A/C post cardioversion). If >48 hours do a TEE or anticoagulate for 3 wks THEN cardiovert when you are sure there is no LA thrombus, then A/C for 4 wks AFTER cardioversion with goal INR of 2-3. If patient is hemodynamically unstableimmediate cardioversion A flutter One automaticity focus 250-300 bpm in atriumregular atrial contractions. Usually 2:1 or 3:1 Atrial to ventricular contractions Causes- COPD, heart disease including coronary dz or heart failure Diagnosis-EKGsaw tooth pattern esp in II, III, avF Tx- same as afib Multifocal Atrial Tachycardia- usually in pts with severe pulmonary dz (COPD) with EKG pattern showing variable P wave morphology and variable PR and RR intervals. (MUST HAVE at least 3 different P wave morphologies for diagnosis) Can be dx by vagal maneuvers or adenosine to show AV block Tx- improve oxygenation and ventilation. LV Function is preserved- CCBs, B Blockers, dig, amio, propafenone (IC antiarrhythmic) LV fxn NOT preserved- dig, dilt or amio. DO NOT CARDIOVERT Paroxysmal SVT: Treatment- Vagal stimulation including Valsalva, Carotid massage, holding breath, cold water immersion of head Acute Tx- IV Adenosine- decreases SA and AV node activity, short duration of action IV Verapamil/ Esmolol/Dig- if preserved LV fxn Cardioversion if drugs not effective Prevention: Pharmacologic therapy with Dig, verapamil or beta blockers Radiofrequency ablation of AV node if episodes are recurrent/ symptomatic Wolff-Parkinson-White- Accessory pathway from atria to ventricles- lacks the AV nodal delaypremature ventricular excitation May lead to Paroxysmal Tachycardia Orthodromic reciprocating tachy- travels through AV node to depolarize ventriclesaccessory pathway back to REdepolarize the atria (Reentry)

Supraventricular Tachys- Fast ventricular rate due to lack of delay at AV nodecan cause hemodynamic compromise Dx-EKG shows narrow complex tachycardia with a short PR interval and a delta wave. Tx-Radiofrequency ablation of re-entrant loop. AVOID DIGOXIN which SLOWS CONDUCTION THROUGH AV NODE VTach-Rapid, repetitive firing of >=3 PVCs in a row btwn 100-250 bpm Normal P waves at their normal Rate, dissociated from QRS Causes include CAD with MI (most common), Active ischemia/hypoTN, Cardiomyopathies, Congenital defects, Prolonged QT, Drug Toxicity Sustained- lasts >30 seconds and is SYMPTOMATIC, associated with hemodynamic compromise such as hypoTN or myocardial ischemia. Is LIFE THREATENINGVFib results Non-Sustained- <30 seconds that are USUALLY asymptomatic. If concurrent Heart Disease or LV dysfxn then increased risk of cardiac death, must evaluate. Prognosis- If non-sustained and not after an MI and no underlying heart disease, prognosis is good. PHYSICAL FINDINGs- CANNON A WAVES and S1 that varies in intensity Dx- Wide, Bizarre QRS that may be monomorphic or polymorphic. DOES NOT RESPOND TO VAGAL MANEUVERS OR ADENOSINE Tx- treat the cause AND: Sustained: o If stable with mild symptoms and Systolic BP>90 then IV amio, procainamide or sotalol o If unstable, DC cardioversion followed by IV amio Non-sustained- only tx if underlying heart dz. Order EP Study, which if +, must place an ICD. Amio if this doesnt work. VFib- multiple foci in ventricles fire rapidly leading to a chaotic quivering of ventricles and no cardiac output. Usually begins as VTach If Vfib is NOT associated with acute MI recurrence is high and pts require prophylactic amio or AICD. If it IS associated with MI within 48 hrs of onset of MI, LONG TERM prognosis is faboriable. No chronic therapy needed in these pts Causes include ischemic heart disease, drugs that cause torsades/Long QT, and AFib with RVR. Dx- EKG shows no P waves or QRS. Tx- IMMEDIATE DEFIBRILLATION (which if not ready, do CPR) by giving up to 3 sequential shocks. If VFib persists, continue CPR and intubate. Push 1 mg IV Epinephrine q3-5mins which increases heart and brain blood flow AND decreases defibrillation threshold. Defibrillate again 60 secs after epi. If Unsuccessful: o Push IV Amio and then try again. If Successful: o Continue IV infusion of the antiarrhythmic that helped.

Long term defibrillator

Bradyarrhythmiaso Sinus Brady- <60 bpm- doesnt become significant clinically until <45 Causes- ischemia, increased vagal tone, antiarrhythmic drugs Symptoms: fatigue, inability to exercise, angina, syncope Tx- Atropine to block vagal tone to SA. If this doesnt help pacemaker o Sick Sinus Syndrome-Persistent, spontaneous sinus bradycardia causing dizziness, confusion, syncope, fatigue, CHF. Pacemaker which causes pacemaker rhythm- spike on EKG Indicationso Symptomatic Heart Block or Bradyarrhythmia o Tachyarrhtyhmias to interrupt rapid rhythms. o AV Block 1st degree- PR interval of >0.2 with QRS after each P wave. NO tx required. 2nd degree Mobitz I- Progressive Prolongation of PR until P wave doesnt conduct- block at AV node. NO TREATMENT Mobitz II- NO prolongationjust dropped QRS o Progress to COMPLETE block. Usually block at HIS PURKINJE system. o PACEMAKER REQUIRED 3rd Degree-Absence of conduction of atrial impulses to ventricles. NO correlation btwn P and QRS. Escape rhythm usually occurs with Ventricular pacemaker establishing heart rate of 25-50. Dilated Cardiomyopathy- most common CM due to insult causing dysfxn of LV contractility. o Death within 5 yrs usually o Causes: CAD with prior MI (most common) Toxic (alcohol, doxorubicin) Metabolic (thiamine/selenium deficiency) Infectious- Chagas, Lyme, HIV Thyroid- hypo/hyper Peripartum CM CVD Pheo/Cocaine (catechol induced) o Clinical Features- symptoms of LV and RV failure. S3, S4 and mitral/TC regurg o Dx- EKG/Echo/CXR consistent with CHF o Tx- CHF tx- digoxin, diuretics, vasodilators, cardiac transplant Remove offending agent. Add in anticoagulation Hypertrophic Cardiomyopathy- most AD mutation, some spontaneous mutations exist o Diastolic Dysfunction develops due to stiff wall. o Worsens upon exertion and any other thing that will increase the heart rate/contractility which also increases the pressures. Also worsens with decreased LV filling (Valsalva) o Dynamic Outflow obstruction if asymmetric hypertrophy of IV septum.

Clinical: DOE, CP, Syncope, Palps, Arrhythmias due to persistently elevated atrial pressures (AFib), Diastolic CHF, SUDDEN DEATH o Signs: Loud S4, Systolic Ejection murmur that decreases with squatting, lying down or straight leg raise, increases with Valsalva or standing, heard at LLSB. o Dx is by Echo o Tx: asymptomatic pts arguably need no treatment but all should avoid strenuous exercise If symptomatic Beta blockers (improve diastolic filling time and reduce contractility, i.e. oxygen consumption) CCB if B blocker doesnt work Diuretics if fluid retention SURGERY- SEVERE disease can take out part of the myocardial septum or replace the mitral valve. Restrictive Cardiomyopathy o Infiltration of myocardium results in impaired diastolic ventricular filling due to decreased ventricular compliance. Due to sarcoid, amyloid, hemochromatosis, scleroderma, carcinoid. o Clinical: Elevated filling pressuresdyspnea and exercise intolerance with right sided signs and symptoms. o Dx- Echo shows thickened myocardium with systolic LV dysfxn. Increased RA and LA size with normal LV and RV size EKG shows low volage,AFib, arrhythmia Definitive diagnosis- Endomyocardial bx o Tx Hemochromatosis- phlebotomy, desferoxamine Sarcoid- glucocorticoids Amyloid- NO TREATMENT DIGOXIN if SYSTOLIC DYSFXN Myocarditis- inflammation of myocardium by viruses, bacteria (GAS/RF, Lyme), SLE, meds (sulfonamides) o Symptoms- fatigue, CP, pericarditis, CHF, death o Dx-ESR AND ELEVATED ENZYMES o Tx- supportive and tx underlying causes Pericardial Diseaseso Acute Pericarditis Causes: postviral (most common- preceded by flulike illness such as Coxsackie, HIV, hepatitis), bacterial (Tb), fungal Acute MI- 24 hrs later (or Dresslers- after weeks) Uremia Collagen Vascular Disease, Neoplasm, Drug induced Lupus, AMyloid, Radiation

Recovery within 1-3 wks Complications- effusion and tamponade (up to 15%) Signs/Symptoms: CP- severe and pleuritic and localized to retrosternum radiating to trapezius ridge and aggravating by laying supine, coughing, swallowing, and deep inspiration Fever, nonproductive cough, pericardial rub (3 components): Atrial Systole, Ventricular Systole, Early diastole. Diagnosis: EKG shows 4 changes IN SEQUENCE: DIFFUSE ST elevation with PR depression ST segment returns to normal T wave inverts T wave returns to normal Tx- Self limited (resolving in 2-5 wks). NSAIDS are mainstay but if NSAIDs dont work, give glucocorticoids. o Constrictive Pericarditis- fibrous scarring of pericardium obliteration of pericardial cavityrestriction of filling during diastole Ventricular filling is OK in early diastole and impeded when heart reaches maximum volume that pericardium can allow (vs tamponade which is ALWAYS hard to fill). Same causes as acute but most are idiopathic Clinical- Patient appears VERY ill and initial symptoms due to elevated systemic venous pressure (edema, ascites) then left sided pressures cause cough, DOE, orthopnea o Dx- EKG shows low voltages, T wave flattening or inversions and left atrial abnormalities Echo/CT/MRI shows thickened pericardium but cannot exclude dx (MRI and CT are obviously better than Echo) CARDIAC CATH- shows = and elevated pressures in ALL chambers. SQUARE ROOT SIGN on Ventricular pressure tracing o Tx- surgical removal of pericardium Pericardial Effusion- any cause of acute pericarditis that can lead to fluid in pericardial space. Can be due to ascites, CHF, Cirrhosis and Nephrotic Syndrome o Clinical: Muffled heart sounds, soft PMI, dullness at left lung base, Friction rub MAY OR MAY NOT BE PRESENT o Dx: Echo is procedure of choice (shows as little as 20 ml of fluid) Water bottle appearance of cardiac shadow on CXR EKG shows low voltages and T wave flattening ELECTRICAL ALTERNANS- alternating variation in direction of EKG wave forms Can determine cause by TAPPING the fluid o Tx- Pericardiocentesis if tamponading. If not, repeat echo in 2 wks Cardiac Tamponade: o RATE of fluid accumulation is impt, NOT amount due to ability of pericardium to stretch. o Decreased stroke volume and COImpairment of diastolic fillingelevation and = pressures of all 4 chambers and the pericardium.

Causes include: Penetrating trauma or iatrogenic (pacemaker insertion or central line placement), Pericarditis or Post MI Free Wall Rupture o Pulsus Paradoxus, Elevated JVP, Hypotension, distant heart sounds o Dx- Echo is most sensitive/specific. EKG shows electrical alternans. o Tx- Nonhemorrhagic- monitor if stable with echo. If due to renal disease do dialysis. If NOT stable, do Pericardiocentesis Hemorrhagic- The answer is NOT pericardiocentesis, it is SURGERY to repair the leak. Mitral Stenosis: usually due to RHD (immune mediated damage)fibrosisLA and Pulmonary Pressure increaseexacerbated by exercise due to increased flow RVF due to chronic Pulm HTNAFib. o Area of valve to create symptoms- 1.5 cm2 o Clinical that you wouldnt already assume: Hemoptysis as LA pressure rises, bronchial veins rupture Thromboembolism Opening SnapLow pitched diastolic rumble with a loud S1 in Left Lateral Decubitus. The closer the opening snap is to S2, the worse the stenosis. o Diagnosis: Echo shows left atrial enlargement with a thickened calcified mitral valve, hockey stick shaped leaflet o Tx- Diuretics, endocarditis PPx, Chronic A/C Surgical only for severe disease- balloon valvuloplasty or comissurotomy or MV replacement Aortic Stenosiso Obstructs LV outflowLVH and eventually LV dilation which leads to mitral regurg due to pulling the annulus apart. o If the valve gets below 0.7cm2, CO fails to increase with exertion Angina o Caused by calcified bicuspid or tricuspid, congenital unileaflet valve, rheumatic fever o Course- Asymptomatic for many years, but once symptomatic, very bad prognosis. Angina- average survival is 3 yrs Syncope- average survival= 2 yrs Heart Failure= Avg survival = 1.5 yrs o Signs- Harsh crescendo-decrescendo systolic murmur in rt 2nd IC space radiating to carotids with an S4, pulsus parvus et tardus, and a precordial thrill o Dx- Echo is diagnostic but CXr would show calcified valve, EKG will show LVH. Cardiac cath is DEFINITIVE diagnosis and allows for measurement of valve area- which if <0.8 cm2 is bad. 3-4 is nml o Tx- Medical therapy SUCKS for this. Must do AV replacement if symptomatic. If asymptomatic NO TX. No balloon angioplasty (lots of recurrent stenoses) Aortic Regurg- Regurg-ed blood increases LV ventricular and diastolic volumedilation of LV and hypertrophycompensation fails leading to increased left sided pressures and Pulmonary Pressures. EF is NORMAL until ADVANCED disease o Acute-need valve replacement. Caused by Infective endocarditis, trauma or dissection o Chronic- survival is 75% at five years but if angina develops survival=4 yrs and if heart failure develops it = 2 yrs

Primary Valvular causes include Ehlers-Danlos, RF, Marfans, SLE Aortic Root Disease includes syphilis, osteogenesis imperfecta, dissection and Bichets. o Clinical: DOE, PND, orthopnea, palps, angina. (Cyanosis and shock if acute) Widened Pulse Pressure, Diastolic Decrescendo murmur at LSB, Corrigans Pulse (water hammer pulse at radial artery), De Mussets Sign (head bobbing) Austin Flint Murmur- low pitched diastolic rumble due to narrowing of mitral valve by aortic regurg. o Dx- Echo in chronic pts to assess need for surgery (size and fxn of LV, dilated aortic root) o Tx Conservative if the regurg is stable (salt restriction, diuretics, afterload reduction, RESTRICT strenuous activities SURGERY is definitive tx- considered in symptomatic or in SEVERE dysfxn on echo. ACUTE REQUIRES IMMEDIATE SURGERY!!! ABE PPx before dental procedures Mitral Regurgo Acute Mitral Regurg causes elevated LA pressureFlash pulmonary edema due to NO time for LA to compensate in size. Hypotension and shock also occur b/c of lack of forward flow. Cause by endocarditis or Papillary muscle rupture o Chronic Mitral Regurg has time to dilate the LA and eventually volume overload of the LV will cause LV to dilate. Pulm HTN occurs too Caused by RF, Marfans or Cardiomyopathy o Clinical that you dont already assume: Holosustolic murmur at apex radiating to back or clavicle AFIB IS COMMON Loud P2, S3 gallop o Dx- Echo o Tx- Medical with vasodilators to encourage more forward flow. Salt reduction, diuretics, dig, and antiarrhythmics Surgical MV Replacement MUST be performed BEFORE LV Fxn compromised TC Regurg- failure of TC valve to close completelyregurg into RA o Usually due to RV DILATION which can be a result of LV Failure, RV infarction, Inferior wall MIor cor pulmonale. o Could also be caused buy TC endocarditis (IV Drug Use), Rheumatic disease (with mitral and aortic), Ebsteins anomaly (Lithium), Carcinoid, SLE o Clinical you dont already know: PULSATILE LIVER Prominent V (ventricular contraction) and rapid Y descent (after V wave) Blowing Holosystolic at LLSB LOUDER WITH INSPIRATION Afib USUALLY present o Dx- Echo which can also measure pulmonary pressure

Tx- Left sided failure tx, endocarditis tx, pulm HTN tx. SEVERE regurg may be surgically corrected (with either Native valve repair, or valvuloplasty. Rarely valve replacement) ONLY if pulm HTN NOT present. MVP- excessive or redundant mitral leaflet tissue (myxomatous degeneration)Click murmur o Common in Ehlers Danlos/Marfans/Osteogenesis imperfecta. o VERY rarely sudden death, rarely Mitral Regurg results o Clinical you dont already know: TIAs due to emboli reported but RARE Midsystolic click with mid to late systolic murmur. STANDING AND VALSALVA INCREASE MURMUR BECAUSE DECREASE IN LV CHAMBER SIZE. Squatting DECREASES murmur b/c it INCREASES chamber size. HAND GRIP- increases this but DECREASES HCM o Dx- echo o Tx- If murmur, then must give Abx ppx. Beta Blockers for CP (if present) Rheumatic Heart Diseaseo Mitral Stenosis due to GAS infxn due to immune mediated damage to valves o Dx- 2 major OR one major/two minor Major= Migratory Arthritis, Erythema Marginatum, Cardiac Involvement, Chorea, SubQ nodules Minor- fever, ESR, Polyarthralgias, prior hx of RF, prlonged PR, ASLO o Tx- Penicillin/Erythromycin for pharyngitis. ACUTE RF is managed with NSAIDS PPx for dental procedures Infective Endocardtitis- usually involves valvular cusps o Acute-Staph aureus on a NORMAL VALVE. Fatal within 6 wks if untreated. o Subacute- Strep Viridans or Enterococcus on DAMAGED valves. Longer time to death. o Native Valve endocarditis- Strep Viridans most commonS AureusS epienterococciHACEK (haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella) o Prosthetic Valves- Staph is most common (S. Epi> S Aureus) (within 60 days post surgery)Strep after 60 days o Complications- cardiac Failure, Myocardial Abscess, Various Solid organ damage from emboli, Glomerulonephritis o Dx- Dukes Criteria: Two major, one major/three minor, or fiver minor required Major: Persistently positive Blood Cx (x3) Visualized valvular deficiency on Echo TEE better than TTE o Tx-4-6 wks of abx IV- start empirically with pen plus aminoglycoside until organism isolated. Nonbacterial Thrombotic Endocarditis-AKA Marantic- associated with metastatic dz. Can embolize to brain or periphery. Sterile deposits of fibrin and platelets along the closure line of the valve.

Libman Sacks Endocarditis- SLE pts involving aortic valve. WARTY vegetations on BOTH sides of valve leaflets. Presents with regurg murmur. o Can embolize o Treat SLE and anticoagulate Atrial Septal Defect: most common is ostium secundum, but can be low in the septum (ostium primum) or high in the septum (sinus venosus) o Can result in Pulm HTN due to LR flows causing increased flow through pulm art o ASYMPTOMATIC UNTIL MIDDLE AGEDOE, fatigue o Heart Sounds- wide, fixed split S2 with mild systolic ejection murmur (flow murmur) in pulmonic area. Also TC diastolic rumble murmur. o Dx- TEE (better than TTE) o Complications- Pulm HTNEisenmengers/ RV failure AFibpossible stroke o Tx- Surgery, only when pulm blood flow:systemic blood flow ratio is >1.5:1 VSD: most common congenital defect. Only large defects will result in pulm HTN in this one and also result in CHF, growth failure and recurrent lower Respiratory infections. Small shunts dont produce ANY problems. o Signs: Harsh, blowing, holosystolic murmur with thrill at LLSB that decreases with valsalva AND handgrip, and gets louder if the defect is SMALLER. Sternal lift (RV enlarged) Pulmonary component of S2 increases as PVR increases CXR shows enlarged PA and enlarged heart. o Dx- ECHO o Complications- Endocarditis, Aortic Regurg, CHF, Einsenmengers o Tx- Endocarditis PP. Surgery only when pulm blood flow:systemic blood flow ratio is >1.5:1 Coarctation of the Aortao Narrowing/constriction of aorta at origin of L subclavian usually. Leads to increaseds LV afterload. o HTN in upper extremities with hypoTN in lower extremities o Mid-diastolic murmur over back o Symptoms: headache, cold extremities, claudication, leg fatigue o Dx- EKG shows LVH and CXR shows notching of ribs o Complications- HTN, Berry aneurysm, Infective endocarditis, Dissection o Tx-SURGICAL decompression or (in select cases) balloon angioplasty PDA- prostaglandins and low O2 maintain the PDA which shunts blood away from lungs usually but outside womb becomes LR shuntpulm HTNrt side failureLATE cyanosis with eventual reversal of blood flow. o Associated with Congenital Rubella, high altitude and PREEMIES o Signs/Symptoms: Heart Failure signs Loud P2 due to pulm HTN LVH due to LR shunt RVH due to Pulm HTN Machinery Murmur Wide Pulse Pressure with bounding pulses

TOES clubbing (more than fingers) b/c toes more likely to be cyanotic Dx- CXR shows increased pulm markings, dilated pulm artery, enlarged heart Tx- If pulmonary vascular disease ABSENT- surgically ligate. If pulm HTN is PRESENT, SURGERY IS CONTRAINDICATED Diseases of the Vasculature: o Hypertensive Emergencies: Systolic >220 or Diastolic >120 IN ADDITION TO end organ damageIMMEDIATE TX needed If elevated BP levels WITHOUT end organ damage, this is hypertensive URGENCY which can be treated slowly over 24 hours. End Organ Systems- Eyes, CNS (AMS or encephalopathy), Kidneys, Heart (angina, MI, CHF), Lungs (pulm edema), Caused by: Noncompliance to therapy Cushings, Hyperaldo, Pheo Drugs (cocaine, LSD), Alcohol withdrawal Eclampsia Vasculitis Clinical: Severe headache, visual disturbances and AMS Workup for HTN with headache: LOWER BP WITH ANTIHTNsive HEAD CT LP Treatment: Lower MAP by 25% in 1-2 hrs. DO NOT RUSH TO CORRECT IMMEDIATELY If Diastolic >130 or if hepatic encephalopathy present- can use IV nitroprusside, labetalol or NG If less danger immediately, can use oral agents such as clonidine, labetalol, captopril or diazoxide Hypertensive URGENCY-lower BP within 24 hours o Dissection HTN is most common predisposing causeTraumaMarfans/Ehlers Bicuspid ValveCoarctationTHIRD TRIMESTER OF PREGNANCY Type A: ascending aorta- more common CP ANTERIORLY (sometimes get aortic regurg) Type B: descending aorta- more common CP INTERSCAPULARLY Pulse/BP asymmetry btwn limbs Can get neuro symptoms (hemiplegia/hemianesthesia) due to obstruction of carotids Dx- widened mediastinum on CXRTEE. Aortic Angio is best test if planning surgery. Otherwise CT/MRI can dx too. Tx- MEDICAL THERAPY IMMEDIATELY ( beta blockers, nitroprusside to get SBP <120). Medical therapy ONLY for Type B. Surgical for Type A. o AAA- localized aortic dilation between renal arteries and iliacs. MORE COMMON IN MEN o o

Causes include HTN, trauma, smoking, vasculitis, Syphilis/Marfans(thoracic) o Clinical you dont already know- mostly asymptomatic Throbbing pain in hypogastrium Expansion and rupture indicated by sudden, severe pain OR: Grey Turners Sign- ecchymosis on the flanks Cullens Sign- ecchymosis around the belly button. TRIAD:ABDOMINAL PAIN, HYPOTN, PALPABLE PULSATILE MASSRUPTURE!!!! CV Collapse, syncope o Dx- U/S for location AND size of AAA. CT in hemodynamically stable o Tx Unruptured- If >5cm resection recommended, If <5cm it is controversial Ruptured- Surgery Leriches Syndrome- atheromatous Occlusion of distal aortabilateral claudication, impotence and absent femoral pulses. PVD- usually coexisting CAD, diabetes, smoking, HLD, HTN, hyperhomocystinemia o Most common sites of occlusion include Hunters Canal (Sup. Femoral Art), Popliteal, Aortoiliac o Clinical- Intermittent claudication (cramping pain reproduced by same walking distance) that is relieved by rest Rest pain- usually felt over distal metatarsals and prominent at night Hanging foot over bed relieves pain due to extra perfusion Less pulses, atrophied muscles, hair loss, thickened toenails, cold Ulceration- secondary to unhealing localized trauma o Dx- ABI >1 is normal. ABI claudication is <0.7. ABI REST PAIN <0.4 Arteriography- gold standard but ONLY needed if surgery is being considered. o Tx- STOP SMOKING STOP SMOKING STOP SMOKING STOP SMOKING Walk to point of claudicationrestwalk for another cycle (called Graduated exercise) Foot Care Therapeutic Lifestyle changes Avoid cold weather Add ASA maybe Surgical Indications- rest pain, ulcerations, affecting QoL or Work (angioplasty or bypass) Acute Arterial Occlusion: Common femoral artery is most common and origin is most commonly from heart (Afib, post-MI, endocarditis, myxoma). o Sx- 6 Ps Pallor, Pulselessness, Paresthesias, Paralysis, Poikilothermia, Pain o Dx- Arteriogram to FIND clot in leg. EKG/Echo to check heart for location that clot was thrown from. o Tx- 6 hrs of ischemia is tolerable on any limb muscle. MUST REESTABLISH PERFUSION WITHIN 6 hrs. If paralysis/paresthesias are ALREADY there, probably needs amputation. IV Heparin should be IMMEDIATE.

Femoral Cutdown and Fogarty Cath. Bypass is for EMBOLECTOMY FAILURE Complication of COMPARTMENT SYNDROME- must assess post embolectomy Cholesterol Embolization Syndrome- usually from proximal atherosclerotic plaque from somewhere in the femoral or iliacs. Usually triggered by catheterization or arteriogram. o Small areas of tissue ischemia (renal, toes, abdominal pain/bleeding) Tx is NOT to A/C. SUPPORTIVE TX ONLY. CONTROL BP Mycotic Aneurysm- from damage to aortic wall during infection. + Blood cultures. Tx= IV Abx AND Sugical Excision Luetic Heart- Syphilitic aortitis complication (men in 4th-5th decade of life) o Aneurysm of Aortic Arch with retrograde extension causing aortic regurg and stenosis of vessels off of aorta. o Tx= IV penicillin and Surgical Repair Venous Stasis Disease (AKA Post-phlebitic Syndrome) o Involves deep, superficial or both with perforating veins connecting the two systems (allowing flow ONLY from superficial to deep) o Underlying cause is FORMER DVTdestruction of valvesvalvular incompetencebackflowdamage to perforator valves which causes superficialdeep flow impairment All this leads to ambulatory venous HTN which causes edema and RBC/ Protein extravastionskin discoloration. Finally, the pressure builds up, overcomes capillary tissue pressue which causes even MINOR trauma to form ulcers ULCERS ARE MEDIAL, FROM THE INSTEP OF FOOT TO ABOVE ANKLE o Clinical-Swelling which causes aching/tight feeling at end of day, relieved by elevation Skin- atrophy, thin, shiny with induration and ulcers that are less painful than arterial ulcers o Tx BEFORE ulcers develop- leg elevation periodically, while avoiding sitting for too long. Compression stockings AFTER ulcers develop- wet-to-dry dressings three times daily. UNNA BOOT q wk-10 days. (compression stocking). Healing occurs in 80%. Split-thickness graft if doesnt heal. Superficial Thrombophlebitis- IF THIS OCCURS IN MULTIPLE PLACES, THINK MIGRATORY (secondary to cancer- esp pancreatic) o General Characteristics- Upper extremities- at site of IV insertion. Lower extremities: at sites of varicose veins (static flow) o Clinical: pain, tenderness, induration, erythema along a vein with a tender cord o Tx- No A/C necessary. Localized- mild analgesic with continued activity Severe (with extension/cellulitis and/or pain) Bed rest, elevation, heat compress, Ambulate with stockings If SUPPURATIVE- drainage required and ABX.

Atrial Myxoma- fatigue, malaise, syncope, low-pitched diastolic murmur that changes with varying positions (diastolic plop). Can embolize and become metastatic. Txsurgery PULMONARY DISEASES: COPDo Chronic Bronchitis- chronic productive cough for at least 3 months of the yr for at least two consecutive yrs Excess mucous production narrows airwaysinflammation and scarring with enlarged mucous glands and smooth muscle hyperplasia obstruction Blue Bloater- overweight, cyanotic, chronic cough/sputum, cor pulmonale in SEVERE disease. No use of accessory muscles o Emphysema- enlargement of air spaces distal to terminal bronchioles due to destruction Centrilobular- smokers- upper lobe destruction limited to respiratory bronchioles Panlboular- in alpha 1 antitrypsin- both proximal AND distal acini at the bases. Due to excess protease (by macrophages and PMNs) or decrease antiprotease (alpha 1 antitrypsin) Tobacco smoke increases number of PMNs and inhibits A1AT. Pink Puffer- thin due to increased energy usage for breathing. Pts lean forward. Barrel Chested. Tacvhypnea with pursed lips. Use of accessory muscles. o Symptoms- cough, sputum, dyspnea Exhalation time >=6 seconds End-expiratory wheezes, tachypnea, tachycardia Cyanosis Use of secondary muscles of respiration Hyperresonance SIGNS OF COR PULMONAEL o Do PFTs if Peak Flow is <350- Low FEV1 with decreased FEV1:FVC (<70% predicted FEV1 is mild. <50 is severe. In btwn is moderate) o Tx STOP SMOKING- Slows the RATE of decline, but NEVER improves back to baseline. Symptoms improve within 1 yr. Inhaled Beta2 Agonists- symptomatic relief. Can use salmeterol Ipratropium- slower onset but longer lasting than beta2s. Combination of the two better than either one alone Corticosteroids- slows down decrease in FEV1 over time but NO benefit to pulmonary function Acute Exacerbations- steroids and moxifloxacin with the above agents. O2 Therapy Indications: o PaO2 55 mm Hg OR O 2 sat<88% OR PaO2 55-59 with evidence of polycythemia or cor pulmonale (due to

pulm HTN from chronic hypoxemia) DESPITE OPTIMAL MEDICASL THERAPY Improves survival. Can be continuous or only during sleep Pulmonary Rehab- goal is to improve exercise tolerance Vaccination- against Influenza (yearly) and Strep Pneumo (q5-6 yrs) o Complications Acute exacerbation due to infection with strep pneumo, hemophilus influenzae, moracxella or mycoplasdma. Or due to noncompliance Secondary polycythemia Cor Pulmonale due to Chronic Hypoxemia causing Pulm HTN Asthmao Airway inflammation and hyperresponsiveness that is reversibly obstructive o Can begin at ANY AGE! o Extrinsic- atopic patient with IgE to environmental triggers. Assoc with hay fever/eczema o Intrinsic- not assoc with atopy or triggers o Tachypnea, diaphoresis, wheezing, accessory muscles, chest tightness o Sign of impending doom- Paradoxical movement of abdomen and diaphragm o Sx worse at night o Dx- Obstructive pattern on PFTs with resolution after bronchodilators with an increase of at least 12% of FEV1 or FVC. (ALWAYS DO PEAK FLOWS IN ED FIRST- fastest method of diagnosis) Peak Flows- Normal for men =450-650 Women= 350-500 >300= mild, >100= moderate, <100=severe Self-monitoring of Peak Flow is impt. Daily if mod. or severe Methacholine Challenge Test CXR necessary to exclude other causes ABG- only if pt is in resp distress. HYPOCARBIA and hypoxemia. If hyPERcarbia occurs, sign of decreasing ventilation. Intubate! o Tx- Albuterol (onset 2-5 mins, duration 4-6 hrs). Inhaled steroids (less side effects than systemic). Singulair (useful for prophylaxins of exercise induced asthma or for moderatesevere persistent) SEVERE Exacerbation (Peak Flow <60% predicted)- albuterol, IV corticosteroid taper. Supplemental O2, ABx if infxn caused, Intubation if in impending respiratory failure. Bronchiectasis- permanent, abnormal dilation and destruction of bronchial walls. Damages cilia. Usually in childhood. o Infection with airway obstruction or impaired defense/drainage mechanisms o Cause identified in < half patients. Less common today due to modern antibiotics o Causes- CF, Infection, airway obstruction o Clinical Features- chronic cough with large amounts of mucopurulent, foulsmelling sputum. Dyspnea, hemoptysis, recurrent/persistent pneumonias o Dx- High resolution CT Scan. PFTs show obstruction. o Tx- Main goal- prevent hemoptysis and pneumonias Antibiotics for acute exacerbations (identified by changes in the amount of sputum, fever, chest pain or sputum color)

Bronchial Hygeine Hydration, Chest PT, Bronchodilators CF- AR condition in Caucasians. Defect in chloride channelthick viscous fluid in respiratory tract, pancreas, intestines, sweat glands o Obstructive lung pattern with Chronic Pulmonary infection (pseudomonas) o Pancreatic Insufficiency and other GI complications o Tx= pancreatic replacement, annual Flu vaccine, Abx if pneumonia develops Lung Cancer: o Two groups include SCLC and NSCLC (25-75%) o Cigarette smoking is biggest risk (linear). ADENOCARCINOMA HAS THE LOWEST ASSOCIATION WITH SMOKING o Asbestos- shipbuilders, construction, mechanics, painting. Synergistic with smoking o Radon- common in basements o COPD is an INDEPENDENT risk factor o Single Pulmonary Nodule workup- after comparing to a previous CXR (if stable over 2 yrs, most likely benign): If suspicion is high, surgical resection is next step. If suspicion is intermediate (based on age (>50) and smoking status), then fiberoptic bronchoscopy is good to r/o malignancy. Do a CXR/CT q few months to evaluate for growth. o Clinical: Local- cough, hemoptysis, obstruction, wheezing, dyspnea, postobstructive pneumonia Constitutional Symptoms- anorexia, weight loss, weakness. Local INVASION SVC Syndrome in 5%, usually SCLC pts leading to facial fullness, facial edema, dilated veins over anterior chest, arms and face. Phernic Nerve Palsy- 1%- destruction of phrenic nerve by tumor Recurrent Laryngeal Nerve Palsy- hoarseness Horners Syndrome- invasion of sympathetic chain by an apical tumor Pancoast Tumor- superior sulcus, usually squamous cell tumorapical tumor involving C8 and T1-T2 causing shoulder pain radiating down arm. o Upper extremity weakness, pain, Horners Mets to bone, brain, adrenal glands, liver Paraneoplastic Syndrome- SIADH (SCLC), ACTH (SCLC), PTHrp (Squamous), Hypertrophic Pulmonary Osteoarthropathy (adeno and squamous)- severe long bone pain Eaton-Lambert- SCLC- similar to myasthenia gravis (proximal muscle fatigue, diminished DTRs, paresthesias) Digital Clubbing o Diagnosis CXR (if stable >2 yrs then benign- could show pleural effsion- which should be tapped), CT Scan (for staging, local and distant mets and LAN),

 o Tx

Sputum Cytology (central tumors only), Fiberoptic Bronchoscope (tissue is REQUIRED for confirmation, useful for central tumors only) Transthoracic Needle Biopsy- PERIPHERAL lesions. Invasive though so selected pts.

SCLC- chemo in both limited and extensive. Radiation ONLY if limited. NSCLC- Surgery IF there is a tissue dx BEFORE (though mets outside chest is contraindication). Radiation as adjunct. o Prognosis- 14% 5 yr survival for ALL lung cancer. Mediastinal Masseso Mestastatic Cancer is the most common cause of mediastinal mass in elderly o Anterior-thymus, thyroid, lymphoma, teratoma o Middle- lung, lymphoma, aneurysms, cysts o Posterior- Neurogenic, esophageal mass, o Clinical: Cough, with hemoptysis if invasive on trachea/bronchi Chest pain, dyspnea Postobstructive pneumonia Dysphagia (compress esophagus) SVC Syndrome Compression of nerves- recurrent laryngeal nerves, Horners, phrenic o Dx- Chest CT (which, if suggestive of benign mass, and asymptomatic pt, can follow) Pleural Diseaseso Effusion- If in the presence of other lung disease, can lead to resp failure. Otherwise, usually asymptomatic Three ways to get it: pleural cells making fluid, drainage of fluid into space, decreased drainage out of the space. Transudative vs Exudative you know. If exudative: Send cell count, glucose, pH, amylase, TGs, cytology, bacteria Protein(effusion:serum) > 0.5 LDH (pleural:serum) >0.6 LDH > two thirds upper limit of normal serum LDH Causes: CHF, Pneumonia, Malignancies, PE, Viral, Cirrhosis Clinical Features- DOE, peripheral edema, orthopnea/PND. Dx CXR shows blunted costophrenic angles (>250 ml fluid) o Decubitus better than PA/Lateral CT Scan- more reliable Thoracentesis- for diagnosis and therapy but can cause pneumothorax. Send for the 4 Cs: cell count, cytology, culture, chemistry If pleural fluid glucose <60 r/o RA. Tx- transudative gets diuretics and Na restriction. Exudative must treat underlying disease. Parapneumonic-

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uncomplicated gets antibiotics Complicated/ Empyema gets chest tube drainage with injection of thrombolytic agents

Empyema Caused by exudative effusion usually due to bacterial pneumonia. Dx- CXR/CT Tx- AGGRESSIVE DRAINAGE of pleura and ABx. Recurrence is common. If severe and persistent, may need to resect a rib w/ open drainage Pneumothorax- air in the normally airless pleural space. Two types: spontaneous and traumatic o Traumatic- often iatrogenic (GET A CXR after Trnasthoracic needle aspiration, thoracentesis and central line placement) o Spontaneous Primary- without underlying lung disease due to subpleural apical blebs High recurrence rate (50% in 2 yrs) Tall young men. Respiratory distress does not occur due to sufficient respiratory reserve. Tx- if small and asymptomatic- observe (should resolve in 10d) o If larger, supplemental O2 and chest tube Secondary- to COPD, TB, CF, neoplasm or asthma- more life-threatening due to lack of pulmonary reserve. Tx- chest tube Tension Pneumothorax- Accumulation of air within pleural space with no escape mechanism. Collapses ipsilateral lung and shifts mediastinum away. o Caused by barotrauma, CPR o Features- hypoTN, distended neck veins, Decreased breath sounds. o Tx- Large bore needle or chest tube drainage. Malignant Mesothelioma- secondary to asbestosDyspnea, Weight loss, and cough with Bloody effusion common. DISMAL PROGNOSIS. Interstitial Lung Disease- inflammatory alveolar wall process with fibroelastic proliferation and collagen depositionFibrosis, impaired gas exchange o Prognosis is variable and depends on diagnosis o Classification Environmental- asbestos, silicosis, berylliosis, coal workers Granulomatous Lung Disease- Sarcoid, Histiocytosis X, Wegeners, Churg Strauss Alveolar Filling disease- Goodpastures, Idiopathic Pulmonary Hemosiderosis, Alveolar Proteinosis Drug-Induced- bleomycin, nitrofurantoin, amio, phenytoin Miscellaneous- IPF, BOOP, Connective tissue disorders (SLE, RA, SS), ARDS, Radiation pneumonitis o Symptoms- Dyspnea, cough, fatigue, bibasilar rales, DIGITAL CLUBBING, pulm HTN o Dx- CXR (findings nonspecific) with diffuse changes (ground glass, reticular) High Resolution CT shows extent of Fibrosis PFTs- restrictive pattern noted with LOW DLCO. Desaturation during exercise

TISSUE BIOPSY REQUIRED which can be done via transbronchial bx on fiberoptic bronch or can be open lung biopsy. Sarcoid- systemic disease with noncaseating granulomas. Almost ALWAYS involves lungs. AA female population. Good prognosis (20% become chronic) o Cardiac disease most common cause of death (but uncommon finding) o Clinical: Constitutional- fever, malaise, weight loss Lungs: dry cough, DOE Skin- Erythema Nodosum, Eyes- Anterior uveitis Heart (5% of cases)- arrhythmias, heart block, sudden death MSK- arthralgias/arthritis, bone lesions Nervous- Bells Palsy, optic nerve dysfxn o Dx- Typical Presentation: young AA woman with constitutional symptoms, resp complaints, erythema nodosum, blurry vision and b/l hilar LAN Skin anergy, Elevation of SERUM ACE Hypercalciuria, Hypercalcemia DEFINITIVE DX- transbronchial biopsy. CXR Staging I- b/l hilar LAN. II- I with parenchymal infiltrates III- diffuse infiltrates without hilar adenopathy (worst one) IV- pulmonary fibrosis/honeycombing o Tx- Spontaneous improvement in 2 yrs in most. Systemic corticosteroids if there are any heart, eye or PFT decline MTX in progressive disease refractory to corticosteroids. Histiocytosis X- chronic interstitial pneumonia due to abnormal proliferation of histiocytes o 90% pts smoke cigs o Dyspnea and dry cough (againoy) o Other complications: spontaneous pneumothorax, lytic bone lesions, diabetes insipidus o CXR is honeycombing and CT shows cystic lesions o Prognosis variable. Tx- corticosteroids or lung transplant Wegeners Granulomatosiso Necrotizing granulomatous vasculitis- vessels of lungs, kidneys, upper airway. URI/LRI, Glomerulonephritis, pulmonary nodules are commonplace o Dx- Tissue bx is gold standard but C-ANCA shows high sensitivity o Tx- steroids and immunosuppressives Churg-Strauss- Systemic vasculitis- Granulomatous dz seen in patients with asthma o Pulmonary infiltrates, rash and eosinophilia due to skin, muscle and nerve lesions o Dx- Eosinophilia and P-ANCA o Tx- steroids Coal Workers Pneumoconiosiso Accumulation of dust in the lungs and tissues reaction to its presence o Simple- causes no disability

o Complicated- fibrosisrestrictive lung disease 2/2 carbon and silica inhalation Asbestosis- DIFFUSE interstitial fibrosis with predilection for lower lobes. o Insidious course; many yrs after exposure o Bronchogenic carcinoma (smoking synergistic) and mesothelioma o CXR shows hazy infiltrates and b/l linear opacities along with Pleural Plaques o NO TREATMENT Silicosis- LOCALIZED and NODULAR peribronchial fibrosis (in the UPPER LOBES) o Can be acute after massive exposuredeath or chronic- years after o Increased risk of Tb if chronic o Mining, Stone cutting, Glass manufacturing o CXR shows EGG SHELL CALCIFICATIONS and Tx is removal from exposure Berylliosis- acute and chronic forms also. Acute is diffuse pneumonitis while chronic is similar to sarcoid (granulomas, skin lesions and hypercalcemia). o Dx- Beryllium lymphocyte proliferation test o Tx- glucocorticoids Hypersensitivity Pneumonitis- inhalation of antigens to alveolichronically leads to restrictive lung dz. o Serum IgG and IgA to inhaled antigen is common o Acutely develops flu like picture with Pulmonayr infiltrates on CXR o Tx- remove offending agent, give gluocorticoids Eosinophilic Pneumonia- fever + periph eos. peripheral pulm infiltrates. Tx- steroids Alveolar Filling Diseases: o Good pastures- U know this. Tx- plasmapheresis, cyclophosphamide & steroids o Pulmonary Alveolar Proteinosis Surfactant-like protein accumulates in alveoli Symptoms- dry cough, dyspnea, rales and hypoxia Ground Glass on CXR. BAT WING CXR (also seen in ARDS and CHF) Lung Biopsy for definitive diagnosis with lavage being the treatment of choice. DO NOT GIVE STEROIDS (increased risk of infection) IPF- male smokers most common with progressive dyspnea and dry cough. Mean survival 3-7 yrs o CXR shows ground glass or honeycombing o Definitive dx is by biopsy but even this may yield nonspecific findings o Tx- none, but supplemental oxygen, steroids +/- cyclophosphamide, Lung transplant have been of use Respiratory Failure o Acute- hypoxia PaO2 <60 and PaCO2 >50. Or hypercapdnia (CO2 >50) How to tell the cause of hypoxemia Need PACO2, A-a gradient, Response to Supplemental O2 A-a gradient normal? hypoventilation o Abnormal? V/Q mismatch (responds to supp O2) or shunting (does not) CNS insult- drug OD, stroke, trauma NM Disease- myasthenia, polio, Guillain-Barre, ALS Upper Airway- obstruction Thorax/Pleura- restriction due to kyphos, flail chest, or hemothorax CVS and blood- CHF, anemia, PE, valvular disease

Lower airways and alveoli- asthma, COPD, pneumonia, ARDS Classifications: Hypoxemia- Low O2 with normal CO2 or low co2. o Causes- anything involving lungsV/Q mismatch/ shunting Hypercarbia- failure of alveolar ventilation o Decreased minute ventilation or increased physiologic deadspace. o Underlying COPD/asthma, CF, bronchitis (lung disease) o Impaired ventilation (neuromuscular, CNS depression) Pathophysiology V/Q mismatchhypoxia WITHOUT hypercapnia Intrapulmonary shuntingno ventilation in perfused areas due to atelectasis or fluid buildup in alveoli or RL blood flow Hypoventilation HYPERCAPNIA WITH 2ndary hypoxemia Increased CO2 productionhypercapnic resp failure Diffusion impairment causes hypoxemia without hypercapnia Clinical: o Symptoms include dyspnea +/- cough o Signs include tachypnea, tachycardia, cyanosisand impaired mentation. Diagnosis: ABG o Hypoxemia- either V/Q, shunt or hypovent Hypercapnia- always hypovent Tx- underlying disorder- bronchodilators, steroids, abx Supplemental oxygen if hypoxemic o Hypoxic Failure: Lowest concentration that provides sufficient oxygenation to avoid toxicity o Hypercapnic Failure: COPD especially (retention of CO2), be careful with supp o2 b/c it will suppress the drive to breath, causing pt to become more hypercapnic NPPV- ONLY if conscious. Otherwise, INTUBATE ARDS- highest risk in pts in septic shock o Diffuse inflammatory process b/l in which neutrophil activation occurs. o Results in massive intrapulmonary shunting of blood due to massive atelectasis, collapse of alveoli and surfactant dysfxnsevere hypoxemia with NO improvement on 100% O2. Interstitial edema and alveolar collapse due to increase in lung fluid, which leads to stiff lungs, increase in A-a gradient, and ineffective gas exchange EFFECTS of increase in fluid are IDENTICAL to cardiogenic pulmonary edema but CAUSE is different: increase in cap permeability is ARDS vs high hydrostatic pressure in cardiogenic o Decreased pulm complianceincreased work of breathing o Increased dead space due to obstruction and dectruction of pulm cap bed o Low FVC low FRC

Causes- sepsis, aspiration, trauma, pancreatitis, drug OD, Intracranial HTN, Clinical Features- Dyspnea, tachypnea, tachy Progressive Hypoxemia- NON responsive to supp o2 Hard to ventilate due to non-compliant lungs o Dx- DIFFUSE B/L INFILTRATES with PCWP <18 and PaO2:FIO2 ratio <=200 Can also do bronchoscopy w/ lavage if acutely ill pt and infxn suspected. o Tx- O2 sat >90%, Mechanical Ventilation with PEEP. Avoid volume overload (PCWP <12-15). Treat infection. NUTRITION. o Complications: Lung Injury- scarring and honeycombing Mechanical Ventilation causing barotrauma or pneumonia Line infection Ileus, Stress Ulcers, MODS Mechanical Ventilationo Goals: maintain alveolar ventilation and correct hypoxemia o Indications: Resp distress or arrest or muscle fatigue Impaired consciousness Metabolic acidosis PaO2 <70, PaCO2>50 o Initially want to rest the resp muscles while preventing barotraumas and atelectasis o Settings: AC- Minute ventilation PRESET. Ventilator delivers breath when patient initiates one but if one is not initiated, the ventilator delivers one anyways. ALL breaths are delivered BY the ventilator. SIMV (synchronous Intermittent mechanical ventilation) Breathe on own over rate WITHOUT assistance from ventilator. Tidal volumes that are OVER the rate are NOT preset , as in AC Initiated in synchrony with the patients normal breath. Appropriate for weaning and support of ventilation CPAP- + pressure delivered continuously but no volume breaths are delivered. PEEP and PRESSURE SUPPORT are the ONLY parameters Pressure Support Ventilation- used during weaning. Pressure delivered with patient-initiated breath to ASSIST breathing. PEEP may be added. Barotrauma like crazy though. o Key Parameters Minute Ventilation- Adjust to patients baseline PaCo2. RR (10-12) x Vt (8-10ml/kg) FIO2= 100% initially with rapid titration down to maintain PaO2 of 50-60 or higher. <60% is usually safe to protect from toxicity Adding PEEP or CPEP allows one to lower the FIO2 I:E ratio- usually set at 1:2 PEEP- 2.5-10 is usually initial. Can be added to ANY of modes of ventilation. Usually used in hypoxic respiratory failure (ARDS).

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Advantages include increased lung compliance and oxygenation. Sie effects include barotrauma and low CO. o Complications Anxiety/Agitation (sedation important with benzos and analgesia with opioids) Suction to prevent aspiration Nosocomial Pneumonia Extubation Barotrauma, O2 toxicity, HypoTN, Tracheomalacea due to prolonged presence of ET tube. Laryngeal damage during intubation Pulmonary HTN: o MAP > 25 mmHg at rest or 30mmHg during exercise o Pathophysiologic Causes: Passive- resistance to pulm venous drainage (Left Sided CHF) Hyperkinetic- High pulm blood flow (LR shunt) Obstructive- Resistance to flow through large PA (PE) Obliterative- Resistance through small arterioles due to parenchymal dz (Primary Pulmonary HTN, CVD, CREST) Vasoconstrictive- Resistance to flow due to hypoxia induced vasoconstriction (COPD, OSA) Increased Intrathoracic Pressure- (PEEP, COPD) o Anatomic Causes: Postcap Causes: Left Sided SHF Mixed Cap and Precap- lung parenchyma/pulm vessels (COPD, ILD, PE) o Clinical: DOE, Fatigue, CP, Syncope Loud P2 (ONLY SIGN A LOT OF TIME) until RV failure occurs o Dx- EKG shows RVH and right atrial abnormalities. Echo shows dilated PA, RA, RV. Abnormal IV Septal movement. Primary Pulmonary HTNo Dx of exclusion due to thickening of arteriolar walls. Unknown cause and poor prognosis o Clinical- same as above o Dx- Cardiac Cath, PFTs showing restrictive pattern, EKG shows RVH o Tx- IV prostacyclins and CCB. A/C with warfarin due to venous stasis Lung Transplant if qualified Cor Pulmonaleo Usually due to COPD but other causes are anything that has lung pathology o Clinical: clubbing, cyanosis, DOE, RV failure, Sternal lift, Polycythemia o Dx- CXR shows enlarged RA, RV and PA EKG- Rt axis deviation, Peaked P waves, RVH Echo- RV dilation, normal LV size o Tx- Tx underlying disorder, use diuretics VERY carefully (preload dependence), Continuous long term O2 therapy Pulmonary Aspiration- Gastric acid, oropharyngeal flora, foreign body/fluids o Aspiration pneumonia occurs in 40% of pts who aspirate- 2-4d later. o Clinical- can have acute resp failure or late resp distress (frothy sputum, hypoxemia, tachypnea, fever). Can lead to obstructionwheeze

Dx- Mimic bacterial pneumonias, Atelectasis possible too Tx- ABCs immediately, supplemental O2, support Abx to cover both anaerobes and aerobes (Clinda/Pen G) If obstructed, early bronchoscopy o Complication- Lung abscess if concurrent poor oral hygiene. Dyspnea- Things that can distinguish btwn lung and heart disease- CXR, Sputum Cx and gram stain, PFTs, ABG, EKG, echo o Distinguish acute (PE, Anxiety, bronchospasm, pneumonia) from chronic (chronic is heart or lung) o Besides cardiac and pulmonary, other causes include: Psychiatric disease (anxiety), Systemic Causes (anemia, sepsis, DKA) Chest Wall Abnormalities- scoliosis, rib fx, ankylosing spondylitis NM Diseases o Dx- Pulse Ox, ABG, CXR, CBC, EKG, Echo, PFTs, V/Q, Bronch o Tx- treat underlying cause. Intubate if: Impending resp fasilure Unable to protect airway Hypoxia <50-60 CO2 >50 Exercise and conditioning may improve perception of dyspnea. Hemoptysis- bronchitis, lung cancer, tb, bronchiectasis, pneumonia, bleeding diasthesis (bold faced is most common) o Massive Hemoptysis- defined as >600ml of blood in 24 hrs. o Protect the airway- intubate if necessary o Bronch can help identify bleeding source. o Tx can be bronch artery embolization o Dx- check for mouth lacs, hematemesis. Look for constitutional symptoms for HIV, Tb. Look for renal disease for goodpastures, wegeners. Look for risk factors of PE CXR- fungal ball, mass, granuloma. Bronch- EVEN if CXR is normal- esp if risk of carcinoma. Look for small tumor on CXR. CT Chest- complements bronch or substitute if bronch is contraindicated o Tx- underlying cause. Suppress cough if aggravating hemoptysis. Correct bleeding diathesis CRC- third most common cancer and almost ALL arise from adenomas o Screening- FOBT has poor sens and spec and PPV of only 20%. DRE detects only about 10% of tumors. Colonoscopy must be done in pt with + FOBT and is diagnostic AND therapeutic. Flex Sig can reach the area where 50-70% of cancers occur. o CEA NOT USEFUL FOR SCREENING o Pattern of Spread- direct extension circumferentially then through bowel wall. Hematogenous to liver, lungs (through vertebral veins). o Risk Factors include: >50yo, Personal hx of Adenomatous polyps (premalignant lesions)/CRC IBD- UC and Crohns BOTH but UC higher risk.

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Family History- Multiple 1st deg relatives, or ANY 1st deg <60yo Polyposis Syndromes FAP AD with hundreds of polyps. Colon ALWAYS involved. Duodenum involved in 90%. Can be in stomach or anywhere else too. Gardners- polyps + osteomas, dental caries, benign soft tissue tumors. 100% Risk of CRC by age 40 Turcots- AR- polyps plus cerebellar medulloblastoma or GBM Peutz-Jeghers- Hamartomas scattered throughout GI tract (78% have in small bowel, 60% in colon). Pigmented spots around mouth. Low malignancy potential. Increased risk for tetes, lung, breast, stomach, ovary cancer. Familal Juvenile Polyposis Coli- small risk of CRC- presents in childhood. HNPCC- Lynch I- early onset CRC (absence of antecedent multiple polyposis). Lynch II- all features of Lynch I plus increased number of other cancers. o Clinical: abd pain, bowel obstruction, weight loss, blood, colonic perf. Right Side bleeds (melena also), Left side obstructs (hematochezia IF bleeding) and is assoc with change in bowel habits (pencil stools-thin) Right Side Triad- weakness, anemia, RLQ mass Rectal Cancer- Hematochezia is most common symptom. Tenesmus and Rectal mass common also. WORSE than colon cancer (more recurs) o Dx- Dukes Criteria- CT of abdomen and CXR. Stage A= muscularis mucosa. Stage B= no nodal involvement but through MM. Stage C= nodes Stage D=mets o Tx- Resect bowel WITH lymphatics AFTER OBTAINING BASELINE CEA Dukes C- Postop chemo. Dukes C RECTAL- both chemo AND radiation postop F/U CT Abd/pelvis and CXR annually, CEA levels q3-6mos, Colonoscopy at 1 yr then q3 yrs Colonic Polyps- found in rectosigmoid, and most asymptomatic. If symptomatic, bleeding is common presentation o Nonneoplastic Polyps- Hyperplastic, Juvenile (under 10 yo- highly vascular and common- should be removed), Inflammatory (pseudopolyps) o Adenomatous Polyps- Tubular (most common), Tubulovillous, Villous. Sessile polyps more likely to be malignant than villous. o Tx- remove polyp Diverticulosis- caused by intraluminal pressure at areas of weakness. Risk factors include family history and low fiber diets. o Clinical: asymptomatic, discovered incidentally on barium enema or colonoscopy. OR: LLQ pain, bloating, constipation/diarrhea IF OBSTRUCTED. o Dx- Barium enema is test of choice. o Tx is high fiber foods to increase stool bulk. o Complications Painless bleeding in 40%. Stops spontaneously usually. Severe req colonoscopy in 5% of patients.

Diverticulitis- which can become complicated to form abscess, fistula, obstruction OR perforation. Recurrence common if treated medically Dx- CT Scan with oral and IV contrast. R/O perf, obstruc by AXR Tx- IV Abx, NPO, IVF. 3-4 day persistence buys tix to OR. Angiodysplasias of the Colon- tortuous, dilated veins in submucosa, commonly bleed in pts >60 yo. 15% can have massive hemorrhage. Diagnosed by COLONOSCOPY. Bleeding usually stops spontaneously but can be coagulated on colonoscopy. Hemicolectomy if necessary Acute Mesenteric Ischemia- almost always have pre-existing CAD o SMA blockage due to 4 causes: Arterial Embolus- from cardiac- sx are sudden and painful Arterial Thrombosis- hx of athroscleorosis elsewhere. Acute event occur on top of the thrombus- sx more gradual and less severe Nonocclusive Mesenteric Ischemia- splanchnic vasoconstriction due to low CO in elderly, occurs in critically ill pts Venous Thrombosis- normal predisposing factors. Sx present for many days, or even wks with gradual worsening. o Clinical Features- severe pain out of proportion to physical Anorexia, Vomiting, MILD GI bleed. Peritonitis, sepsis may present Infarcted Bowel- hypoTN, tachypnea, lactic acidemia, AMS, fever. CHEC THE LACTATE LEVEL IF AMI IS SUSPECTED. Do Mesenteric Angiography for definitive diagnosis. Would see thumbprinting on basrium enema AXR due to thickened mucosal folds o Tx- IVF and ABX. Papaverine infusion into SMA is tx of choice. OR direct intraarterial infusion of thrombolytics Heparin in venous one. Surgery if peritonitis develops CMI- atherosclerotic disease leading to abdominal angina which is dull and postprandial. Weight loss is common. Dx- Mesenteric Angio. Tx- Surgical revascular Ogilvies Syndrome- NO mechanical obstruction, but radiography shows signs of obstruction. o Causes- Recent surgery, trauma, serious illness (cancer/sepsis) o OBSTRUCTION MUST BE EXCLUDED o Tx- supportive- IVF, electrolytes DECOMPRESSION with NGT or ENEMAS (ESP IF DIAM >10 cm-rupture risk). If these methods fail, must do colonoscopic decompression and last resort is colostomy. C-Dif Colitis- Toxin production is main cause. Clinda, Ampicillin and Cephs are most common causative agents o Usually begin DURING 1st wk of abx. o Clinical: diarrhea (no blood/mucous), crampy pain and Toxic megacolon (TMC) o Dx- C Dif toxin in stool. Flex sig can show pseudomembranes. AXR to r/p TMC o Tx- d/c abx, metronidazole + oral vanc. Cholestyramine can improve diarrhea o Complications: Toxic Megacolon, Perforation, Electrolyte disturbances Colonic Volvuluso Twisted bowel around its mesenteric origin resulting in possible obstruction or vascular obstruction (necrosisperforation)

Sigmoid 75% (illness, age, CNS disease) and cecal 25% (congenital lack of fixation of rt colon) o Clinical: acute colicky pain, obstipation, abd distention, N/V, anorexia o Dx- Abd plain film shows omega loop sign for sigmoid volvulus or cecal volvulus shows coffee bean sign (air fluid level) Sigmoidoscopy preferred due to diagnostic AND therapeutic abilities. Barium Enema (ONLY if NOT suspecting strangulation) o Tx- Sigmoidoscopic decompression or emergent surgery Liver Cirrhosis- fibrosis, disruption of liver architecture, nodules leads to portal HTN & Hepatocellular failure (synthetic- albumin & PT). Diagnostic gold standard is biopsy. o Childs Classification- assesses fxnl reserve of liver (A-C, C being worst) o Two most common causes- Alcohol and Hep C. o Complications Portal HTN leading to bleeding. Treat with TIPS to lower portal pressure Varices- esophageal, gastric, duodenal lead to bleeding which leads to melena, hematemesis and hepatic encephalopathy. Tx- Stabilize with fluids, do endoscopy and give beta blockers long term to prevent further bleeding Ascites- fluid into peritoneal cavity leading to distention, shifting dullness and fluid wave. U/S detects as little as 30 mls of fluid and paracentesis (indicated in new onset or worsening ascites or suspected SBP) can determine cause. Serum-Ascites albumin Gradient (Serum-Ascites) >1.1 is portal HTN. <1.1 other causes considered Tx- bed rest, low Na diet, diuretics, therapeutic paracentesis, TIPS. Hepatic Encephalopathy- toxic metabolites (ammonia, GABA) accumulate. Occurs in 50% of cirrhotics. Alkalosis or hypokalemia, sedating drugs, GI Bleeds, Infection can all set this off Clinical Features- AMS, ASTERIXIS, Rigidity, hyperreflexia, Musty odor of breath (Fetor hepaticus) Tx- Lactulose prevents ammonia absorption. Neomycin kills bacterial flora in gut. Limit protein in diet Hepatorenal- End Stage Liver causes renal failure due to renal hypoperfusion. Worsened by diurections. FUNCTIONAL renal failure that DOES NOT respond to fluids. Azotemia, oliguria, hyponatremia/hypoTN, low urine Na ONLY tx is LIVER TX. SBP- up to 20% of patients that are hospitalized for ascites High mortality and high recurrence. Organisms: E Coli, Kleb and Pneumococcus Clinical: pain, fever, vomiting, rebound tenderness, and may lead to sepsis Dx: Paracentesis shows >500 WBC, >250 PMNs Tx: Broad Spectrum AbxCxNarrow Spectrum

REPEAT PARACENTESIS IN 24-48 hrs. HyperEstrinism- spider angiomas, palmar erythema, gynecomastia Hypocoagulability- decreased clotting factorsIncreas PT, PTT unable to tx with Vitamin K. Must give FFP HCC o Tx- underlying cause (alcohol or Hep C). Manage complications. Liver tx (must abstain alcohol 6 mos) Wilsons Disease- AR disease of copper metabolism- deficiency of ceruloplasmin (necessary for copper excretion). Copper accumulates in kidney, cornea and brain. o Present btwn age 5-35 Liver Disease- hepatitis, cirrhosis, or hepatic failure Kayser-Fleischer Rings CNS Extrapyramidal signs- parkinsonian sx, chorea, drooling (basal ganglia) Psychiatric Disturbances- depression, neuroses, psychosis. Renal Involvement- aminoaciduria and nephrocalcinosis o Dx- decreased ceruloplasmin with liver bx showing copper elevation o Tx- penicillamine, Zinc (prevents uptake of dietary copper), Liver tx. Hemochromatosis- AR disease of excess iron absorption which lead to excess iron free radical production fibrosis in involved organs (liver, pancreas, heart, joint, skin) o Early in disease, only MINOR elevations in liver enzymes. Order iron studies then get a liver biopsy for iron. o Symptoms include liver disease, abdominal pain, cardiac arrhythmias, brittle diabetes, impotence (testes involved), bronze skin o Complications include Cirrhosis *increased 200x risk of HCC* , CHF/ Arrhythmias, Arthritis (2nd and 3rd MCPs), Diabetes, Hypogonad, hypothyroid o Dx- Elevated iron, ferritin, % sat, with low TIBC. LIVER BX REQUIRED FOR Dx. o Tx- Phlebotomy. Hepatocellular Adenoma- young women on OCPs or men on steroids- benign tumor o Asymptomatic usually- incidental. LOW malignant potential, but may rupture. o Dx- CT, U/S or arteriography (most accurate, but invasive) o Tx- D/C OCPs, resect tumors >5 cm. Cavernous Hemangiomas- vascular tumor- small and asymptomatic. MOST COMMON o RUQ Pain/Mass as tumor grows (preggos or OCP use) o Complications- rupture, obstructive jaundice, CHF secondary to LARGE AV SHUNT, GASTRIC OUTLET OBSTRUCTION (ALL UNLIKELY UNLESS LARGE) o Dx- U/S, CT with IV contrast. BIOPSY CONTRAINDICATED o Tx- consider resection ONLY if large (high rupture risk). Otherwise, no tx. Focal Nodular Hyperplasia- Benign liver tumor. NO ASSOCIATION with OCPs. No malignant potential. Asymptomatic hepatomegaly. No Tx necessary HCC- 80% of primary liver cancer. Africa and Asia most common. o NonFibroLamellar- Hep B or C, usually unresectable o FibroLamellar- NOT assoc with Hep B or C, resectable (longer survival), young adults commonly o Risk Factors: cirrhosis, aflatoxin/vinyl chloride, A1AT, Hemo/Wilsons, Schisto, Hepati Adenoma, Cigs

Clinical: Abd pain, weight loss, fatigue, anorexia, Cirrhotic symptoms, Paraneoplastic Syndromes (Erythro/thrombocytosis, hypercalcemia, carcinoid, hypoglycemia, high cholesterol) o Dx- Liver Bx. U/S abd, CT chest to assess staging. AFP BEFORE surgery. o Tx- Liver resection or transplantation NASH- no hx of alcohol use, but identical histo to alcoholic liver dz. OBESE, HLD, DM associations. Usually asymptomatic and benign (cirrhosis can develop in 10-15%). No clear tx. Gilberts- AD condition- decreased UDP Glucoronyl transferase activity. Causes isolated indirect bili elevation, exacerbated by fasting, fever, alcohol and infection. Liver bx results normal. No tx necessary Hemobilia- blood in the duodenum via common bile duct due to bleeding ANYWHERE in the biliary tract. Usually due to trauma but can be due to surgery, tumors or infxn. o GI bleeding (melena usually), Jaundice and RUQ pain o Dx- Arteriogram. Upper GI endoscopy shows blood out Ampulla of Vater. o Tx- volume replacement. Surgery to ligate arteries if necessary Liver cystso Polycystic Liver Cysts- AD and assoc with ADPKD (usually cause of death). Usually asymptomatic but sometimes pain or mass in RUQ. Tx unnecessary o Hydatid Cysts- Echinococcal infection. Right lobe of liver. Large cysts cause RUQ pain, ruptureanaphylactic shock. Tx= Surgical Resection. Mebendazole after surgery Liver Abscesses: o Pyogenic- usually due to biliary tract obstruction. E. Coli, Kleb, Proteus, Enterococcus, anaerobes. Fever, malaise, anorexia, weight loss, N/V, RUQ pain, jaundice Dx- CT or U/S Tx- IV Abx and PCT drainage- Fatal if untreated. o Amebic- most common in men 9:1, with homosexual men mostly. Caused by Entamoeba Histolytica which reach liver by portal vein. Dx-Serology or Stool for O and P. Tx- IV Metronidazole, aspiration if necessary (rupture risk). Budd-Chiari- Liver disease due to hepatic venous outflow obstructionmicrovascular ischemia. Portal HTN develops. Rarely severe leading to acute liver failure o Causes: hypcoagulability, myeloproliferative disorders, pregnancy, inflammation, infection, cancers, trauma. o Clinical- heptomegaly, ascites, RUQ pain, jaundice, bleeding. o Dx- Hepatic Venography o Tx- Surgery usually necessary (balloon angioplasty) with stent placement Jaundice- jaundice becomes clinical at tbili >2. o DARK URINE ONLY SEEN WITH CONJUGATED BILIRUBIN (WaTER soluble) o Unconjugated form is TOXIC to neurons. Cannot be excreted in urine either. Liver Enzymes- ALT more sensitive, AST more specific o Mild elevation- acute alcoholic hepatitis or chronic viral hepatitis o Moderate- (high hundreds to thousands)- acute viral o Severely- >10k- hepatic necrosis due to severe viral, shock liver or acetaminophen

Mnemonic for ALT/AST elevation in asymptomatic: Autoimmune, Hep B/C, Drugs, Ethanol, Fatty liver (triglycerides), Growths (tumor), CHF, Iron/copper/A1AT AlkPhos- bile stasis. If >10x normal, think EXTRAHEPATIC obstruction or intrahepatic cholestasis. If elevated, measure GGT to check for bone/intestinal origin vs liver. Clotting- Synthesis of I, II, V, VII, IX, IX, X, XII, XIII. If PT is prolonged, this is advanced liver disease. Things you dont know about stones: o Cholesterol stones also associated with Native American Ancestry and CF o Pigment Stones assoc with hemolysis or alcoholic cirrhosis o Mixed stones exist (majority of stones) o 1/3 pts with biliary colic develop acute cholecystitis within 2 yrs o Boas Sign- referred right subscapular pain of biliary colic. o Pain in acute cholecystitis is due to wall inflammation, vs pain in biliary colic which is gallbladder contraction against an obstructed cystic duct. o Elective chole for pts with recurrentbiliary colic Complications of cholecystitis: o Gangrenous cholecystitis o Perforated Gallbladder o Emphysematous Cholecystitis o Cholecystenteric Fistulagallstone ileus o Gallbladder Empyema Acalculous Cholecystitis- no stones. Usually idiopathic seen in pts with severe illness including dehydration, burns, sepsis, and severe trauma. EMERGENT CHOLE. If pt not stable, emergent cholecystostomy. Choledocholithiasis- gallstones in the CBD. Primary stones (usually pigment stones) originate in the CBD while secondary stones (usually cholesterol or mixed) start in the gallbladder and end up in the CBD. o RUQ Pain, jaundice with possible development of cholangitiis, obstructive jaundice, acute pancreatitis, or biliary cirrhosis. o Dx- T-bili, Alk-P, D-bili elevated. ERCP IS GOLD STANDARD (NOT U/S- only detecs 50%) o Tx- ERCP with sphincterotomy and stone extraction with stent placement. If unsuccessful (10%), do lap choledocholithotomy. Cholangitis- due to choledocholithiasis, pancreatic neoplasm, stricture, ERCP. o RUQ pain, fever, jaundice. + hypoTN, AMS o Must get blood cultures, IVF, IV ABx, Decompress CBD. o Dx- U/SCholangiography via ERCP (if normal duct on ultrasound) or PTC (if dilated duct on ultrasound). o Hepatic Abscess= most serious complication of cholangitisGallbladder Carcinoma- most adenocarcinomas and occur in elderly. Usually assoc with gallstones, but also caused by cholecystenteric fistula or porcelain gallbladder. o Clinical: Extrahepatic bile duct obstruction signs. o Bad Prognosis, but can do chole or radical chole (with liver wedge resection and LN dissection) PSC-EXTRAhepatic, and/or intrahepatic bile ducts- thickened walls and narrowing of lumens. Leads to cirrhosis, Portal HTN, Liver Failure. STRONG association with UC.

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o Presenting Symptoms: jaundice and pruritisobstructive jaundice o Dx- ERCP and PTC (bead like structuring of bile ducts) o Tx- no curative tx- LIVER TRANSPLANT, but can do stent placement if necessary. o Complications- 20-30% get cholangiocarcinoma. 15% get cholangitis recurrent. PBC- INTRAhepatic bile ductsportal inflammation and scarringEnd Stage liver failure o Autoimmune and associated with other autoimmune diseases- middle age women o Pruritis early, jaundice late. Fatigue, RUQ pain, Xanthomata, Xanthelasma. o Dx-cholestatic LFTs, Positive Anti Mitochondrial Antibody, hallmark. LIVER bx confirms. o Random facts: Elevated cholesterol/HDL, IgM. o Tx- cholestyramine for pruritis, ursodeoxycholic acid (bile acid) slows progression, but liver tx is only curative tx. Cholangiocarcinoma- Most are adenocarcinomas- usually in 7th decade of life. o Proximal 1/3 of CBD is Klatskin, distal extrahepatic, intrahepatic (in order of freq) o Survival <1 yr. o Usually due to PSC, but clonorchis, UC, choledochal cysts also. o CLINICAL: obstructive jaundice with dark urine & acholic stools with pruritis o Dx- PRC or ERCP for dx and resectability. If unresectable (proximal), stent placement can occur for obstruction Choledochal Cysts- cystic dilations of tree more common in women. o Epigastric pain, fever, jaundice, RUQ mass. o Complications: Cholangiocarcinoma (most feared), hepatic abscess, pancreatitis/cholangitis o U/S is best non-invasive test. ERCP for definitive o Tx- surgery- resection with biliary enteric anastomsis. Bile Stricture- usually due to iatrogenic injury but recurrent choledocholithiaisis common too. o Clinical- obstructive jaundicesecondary biliary cirrhosis, liver abscess or ascending cholangitis (all life threatening)_ o Tx- endoscopic stenting or bypass if endoscopic tx fails Biliary Dyskinesia- motor dysfxn of sphincter of oddibiliary colic with no gallstones. Dx= HIDA. Once gallbladder is filled, give CCK IV and check for low EF of gallbladder. o Tx- lap chole or endoscopic sphincterotomy Carcinoid- neuroendocrine related and secrete serotonin. Tumors can be in appendix, small bowel, rectum, bronchi, kidney, pancreas. 10% develop carcinoid syndrome. (flushing, diarrhea, sweating, TIPS). SIZE of tumor is prognosticator of metastatic potential. Tx- surgical resection Acute Pancreatitiso Inflammation from prematurely activated enzymes invoking autodigestion. o Causes- GET SMASHED- Gallstones, ethanol, trauma, scorpion sting, mumps, steroids, autoimmune, hypertrigs, ERCP, Drugs o Clinical- epigastric abd pain, radiating to back of steady, severe, dull onset. Worse after meals.. Fever, tachy, distention, ABSENT BOWEL sounds. Cullens (periumbilical), Gray Turners (flank), Fox (inguinal ligament). o Dx- amylase/lipase, LFTs (for gallstone cause), Ransons Criteria (glucose, age, ldh, ast, wbc, calcium, hematocrit, O2 Sat, BUN, Base deficit, Sequestratio

U/S for stones or pseudocysts, CT is most accurate diagnostic test. CT Indicated in SEVERE pancreatitis. o Tx- NPO, IVF, Pain Control, NGT if nausea. o Complications: Necrosis which may be sterile or become infected (high mortality-50%), Distinguish between the two by CT-guided PCTA with gram stain/Cx Pseudocysts- 2-6 wks after acute attack. Can occur at distant sites from pancreas. Can rupture, infection, GOO, fistula or hemorrhage. Dx- CT Tx- observe <5cm, drain >5cm Hemorrhagic Pancreatitis- Three signs as above. Dx with CT w/ IV con ARDS- HIGH mortality Ascites/Pleural Effusion- due to inflammation of peritoneal surfaces Abscess- less life threatening than infected pancreatic necrosis. Occurs 4-6 wks later Chronic Pancreatitis- diagnostic sign is calcifications on AXR. Triad- steatorrhea, DM and calcifications. o Fibrosis of pancreas due to common acute pancreatitisStrictures of ducts o Chronic alcoholism is the cause in >80% of cases. o Clinical- severe epigastric pain w/ radiation, with N/V, aggravated by eating/drinking. Weight loss due to malabsorption. DM, Steatorrhea. o Dx- CT SCAN IS DX TEST OF CHOICE (more sensitive to calcifications) o Tx- analgesia, NPO, PPI to stop acid secretion (which would destroy the exogenous pancreatic enzymes), pancreatic enzyme replacement (decrease CCK stimulation of pancreas), Insulin, Frequent-small volume- low fat meals. Surgery to relieve abd pain- pancreaticojejunostomy or whipple. o Complications- narc addiction, DM, steatorrhea, pseudocysts, duct dilation, CBD OBSTRUCTION (due to fibrosis), B12 deficiency, Effusions, Pancreatic cancer. Pancreatic Cancer- elderly and African Americans. 75% in head. o Risk Factors- cigs, alcohol, chronic panc, DM, o Clinical- Painless jaundice is NOT common. 90% of pts present due to vague, dull abd pain. Weight loss, DM , Migratory Thrombophlebitis, Courvoisiers Sign (palpable, nonpainful gallbladder) o Dx- ERCP- to distinguish from other obstructing cancers. CT to assess stage, spread. CA-19-9 and CEA- tumor markers o Tx- Whipples is ONLY hope for a cure but can do stenting for palliation Aortoenteric Fistula- after aortic surgery, rare but fatal cause of hematochezia. Usually involves duodenum. Perform endoscopy or surgery during window of slow bleed that will eventually hemorrhage and kill the patient. Lower GI Bleed in patients >40 is cancer until proven otherwise 80% of UGI bleeds stop spontaneously and only need supportive therapy ALWAYS ask pts with GI Bleed if they take NSAIDs, aspirin or A/C Esophageal cancer o Two pathologic types (SCC and adeno). SCC has survival of 20% at 1 yr and 5-10% at five yrs.

Higher in AA men, alcohol and tobacco, diet (betl nuts, nitrosamines), HPV, achalasia, Plummer-Vinson. Adeno- Caucasian men. GERD and Barrets. Poor prognosis also Stage I- invasion of lamina propria or submucosa-. Stage IIa- muscularis propria or adventitia IIb- muscularis propria w/ positive regional nodes III- adventitia with regional nodes OR invades adjacent structures o Clinical- dysphagia, weight loss, anorexia, odynophagia (extraesophageal involved) o Dx- Barium SwallowUpper endoscopy with bx to confirm. o Tx- Palliation. Surgery if Stage 0,1,2A, but do chemo + radiation prior to surgery. Achalasia- Motor dysfxn of LES with abnormal peristalsis. ABSOLUTE CRITERIA INCLUDE: incomplete relaxation of LES and Aperistalsis of esophagus. o America- Idiopathic or adenocarcinoma of stomach.Worldwide- Chagas Disease o Clinical Dysphagia (solids=liquids), eat slow and drink liquids to wash down food Regurgitation- food gets stuck in esophagus and comes back up Chest Pain, weight loss, ASPIRATION SQUAMOUS CELL CARCINOMA OF ESOPHAGUS o Dx- Barium swallow- birds beak, EGD to r/o gastric cancer as cause. Manometry confirms o Tx- chew food well, elevate HOB. Medical therapy- Antimuscarinics (dicyclomine), Sublingual Nitro, nitrates or CCBs can all improve swallowing in early achalasia. Can inject botulinum toxin during endoscopy q 2 yrs. Can do surgical myotomy or pneumatic balloon dilation. NO CURE- only PALLIATION Diffuse Esophageal Spasm- nonperistaltic contraction of esophageal body similar to CARDIAC chest pain (most pts undergo cardiac workup with negative cath). Several segments of esophagus contract simultaneously. SPHINCTER FXN NORMAL. o Pain may radiation to jaw!!! o Dysphagia common, regurg UNCOMMON. o Dx- Manometry (nml sphincter w/ simultaneous weird contractions) o Tx- no completely effective tx. Nitrates, CCBs. TCAs provide symptomatic relief. NO ESOPHAGOMYOTOMY. Hiatal Herniao Type 1 is sliding- 90% of all hernias. Associated with GERD. Benign. Tx is tx for GERD o Type II is paraesophageal- <5% cases. Herniated into thoracx but GEJ stays below diaphragm. Can strangulate. Must be surgically repaired. o Type III is mixed and treated like a type II. o Dx- Barium Swallow or Endoscopy Mallory-Weiss- mucosal tear just below GEJ due to retching. Hematemesis. EGD is diagnostic. Most cases stop bleeding without any tx. Tx is surgery or angiographic embolization (angiographic).

Plummer-Vinson- Esophageal web, iron deficiency anemia, koilonychia. 10% develop SCC of oral cavity, hypopharynx or esophagus. Considered Premalignant. Txesophageal dilation and iron supplements Schatzkis Ring- distal ring in esophagus that is always accompanied by sliding hiatal hernia. Asymptomatic usually but mildmoderate dysphagia can occur. Symptomatic with no reflux earns themselves some esophageal dilation. o If reflux, consider fundop o Due to ingestion of alkali, acids, bleach, detergents. o Increases chances of esophageal cancer. o Tx- If full thickness necrosis (alkaline usually) then must do esophagectomy. AVOID VOMITING and ALL ORAL INTAKE. Give steroids for inflammation. Esophageal Perf- blunt trauma, iatrogenic (endoscopy) or Boerhaaves. o Pain, tachy, hypoTN, Hammans Sign (mediastinal crunch on breathing), Pneumothorax, Effusion. o Dx- Soluble Gastrograffin swallow o Tx- IVF, NPO, ABx, H2 blockers if perforation is SMALL. If large, do surgery (within 24 hours or mortality increases) PUD- H. Pylori, NSAIDs, ZE Syndrome. Smoking. o Aching/gnawing epigastric pain, nocturnal symptoms o Duodenal ulcers caused by higher basal levels of acid vs gastric is due to decreased defensive factors. Type I is less curvature, II is gastric AND duodenal, III is prepyloric, IV is near GEJ. o If you suspect ANY of the complications, must do diagnostic studies, but if there is no suspicion of complications, give PPI prophylactically. o Dx- Endoscopy (can also do bx for malignancy or H pylori, or tx bleeding) Barium Swallow less reliable Serum Gastrin if ZE suspected o Tx- Medical- d/c ASA/NSAIDs, Avoid eating before bed. Acid Suppression, H Pylori tx, Sucralfate to cover ulcers. Surgery only to treat complications Acute Gastritis- inflammation of gastic mucosa due to NSAIDs, H Pylori, alcohol, cigs, or caffeine. o No relationship between eating and pain. If no suspicion for complication or red flags then can do empiric acid suppression. Can do EGD if no response (4-8 wks) or if red flags Chronic Gastritis- most common cause is H Pylori, though autoimmune is second (antiparietal and anti-IF Abs). Most are asymptomatic. May look like PUD, which is a complication of this dz, along with gastric carcinoma, Gastric Cancer- majority are adenocarcinomas and common in Japan. Abdominal pain, early satiety, melena, guaiac +. o Ulcerative Carcinoma- ulcer though ALL layers o Polypoid Carcinoma- solid mass projects into stomach lumen o Superficial Spreading- best prognosis o Linitis plastica- leather bottle, through all layers early, thick rigid wall. WORST ONE o Dx- Endoscopy with bxStaging with Abdominal CT. o Tx- Resect w/ >5cm margins o Blumers Shelf- mets to the rectum palpable on rectal exam

o Irishs Node- mets to the left axillary nodes. Hyperthyroido Graves- Autoimmune stimulation by thyroid stimulating globulin. Extra synthesis of thyroid hormone. Radioiodide scan shows diffuse uptake Diffusely (symmetrically) enlarged thyroid gland, with a bruit present Pretibial myxedema, exophthalmos, bruit- all specific for graves. o Plummers Disease- toxic multinodular goiter- hyperfunctioning areas (decreased TSH levels). Rest of thyroid doesnt function. Pathcy appearance on uptake scan. Common in ELDERLY pts o Subacute Thyroiditis- exquisitely tender gland after a viral illness o Hashimotos Thyroiditis- can cause TRANSIENT hyperthyroid o Other causes- transient postpartum thyroiditis, iodine induced. o Hyperthyroid in elderly- could manifest as weight loss, weakness or A FIB. Clinical Features of hyperthyroid include weight loss, heat intolerance, brisk reflexes, sweating, tremor, palpitations, insomnia/irritability o Extrathyroidal: cardic arrhtyhmias, warm, moist skin Dx of Hyperthyroid- Serum TSH low. Next get T4. o Radioactive T3 uptake- gives info about Thyroid binding globulin (which is increased in pregnancy, liver disease, OCPs and ASA use. Give resin which binds all the radioactive T3 that TBG DOESNT BIND. Differentiates btwn true hyperthyroid and increases in TBG. If true hyperthyroidism, all spots will be taken up on TBG already and all the infused radioactive T3 will bind back to the resin. Tx of hyperthyroido PTU/Methimazole inhibit T4 synthesis. PTU also inhibits peripheral conversion to T3. Major S/E is agranulocytosis o B-Blockers- symptomatic management o Radioactive Iodine Ablation- most common tx for Graves in US. Complication is hypothyroidism. Administer a second dose in 6-12 mos if first doesnt work. CONTRAINDICATED DURING PREGGO/BREASTFEEDING o Surgical- subtotaleffective but possible permanent hypothyroid/hypoPTH, recurrent laryngeal nerve injury, recurrence of hyperthyroid Must monitor calcium o Beta Blocker firstMethimazole (if not pregnant with Graves), taper beta blocker over 4-8 wkscontinue methimazole 1-2 yrsget TSI checked If pregnant and Graves- PTU is preferred. Thyroid Storm- life threatening complication of thyrotoxicosis (hyperthyroid). o Exacerbation of manifestations of hyperthyroidism. Usually a precipitating factor like DKA or infxn. 20% die or end up in a coma. o Fever, tachy, agitation, psychosis, confusion, GI symptoms, confusion, GI Symptoms o Tx- IVF, cooling blankets, GLUCOSE + antithyroid (PTU q2h) and iodine (to inhibit TH release) Hypothyroido Insidious onset and many times asymptomatic o Causes include Hashimotos, Iatrogenic and secondary hypothyroid. o You know the signs/symptoms already

Dx- High TSH in primary, low TSH in secondary hypothyroidism. Hashimotos has anti-microsomal antibodies. Lab abnormalities include high LDL, low HDL, and normocytic anemia o Tx- Levothyroxine- check TSH frequently Myxedema Coma- rare state that presents with depressed consciousness, hypothermia, and respiratory depression. Develops after YEARS of untreated hypothyroid and triggered by infection, cold, narcotics Subacute Thyroiditiso Follows viral illness- transient hyperthyroid (leakage of enzymes) followed by euthyroid state and then hypothyroid (due to depletion of enzymes) o PAINFUL, TENDER THYROID o Dx- Radioiodine uptake LOW (damaged cells cant trap iodine) o Tx- USE NSAIDS AND ASA FOR MILD. For severe pain, corticosteroids. Recovery occurs in 1 month to 1 year Subacute Lymphocytic Thyroiditis- painless transient thyrotoxic phase (2-5 mos) followed by hypothyroid phase which is self-limited. o Differentiated from Graves by low radioactive iodine uptake. Similar to subacute thyroiditis except without the pain Chronic Lymphocytic Thyroiditis (Hashimotos)- autoimmune thyroid more common in women. Commonly has antithyroid antibodies. o Goiter is most common feature. 20% of cases have hypothyroid. o Dx- TFTs are NORMAL unless hypothyroid is present. Anti-TPO or Anti-Thyroglobulin o Tx- Thyroid hormone Thyroid Nodules- FNA is the ONLY test that can reliably differentiate between benign and malignant nodules. o Cancer in 10-20% nodules. Solitary nodules- cancerous or benign. o Detectable on palpation MUST be at least 1cm in diameter o Malignant signs: fixed, firm, irregular, solitary, radiation in past, rapid development, vocal cord paralysis, adenopathy, elevated calcitonin. o Dx FNABenignObservation/Repeat FNA if persists FNAIndeterminateThyroid ScanHot noduleclose observation with periodic thyroid studies FNAindeterminatethyroid scanCold NoduleLobectomy FNAMalignantSurgery FNA is reliable for all cancers EXCEPT FOLLICULAR o Thyroid Ultrasound differentiates solid from cystic but most cancers are solid. Cannot distinguish btwn benign and malignant. Thyroid Cancero Head and neck radiation during childhood. o Gardners Syndrome for papillary cancer o MEN Type II- medullary cancer o Papillary Cancer- 70-80% of all thyroid cancers but least aggressive- slow growth/slow spreading. Spreads via lymphatics in neck and mets to cervical nodes. Positive iodine uptake. ESPECIALLY IN RADIATION.

Tx- lobectomy with isthmusectomy. Total thyroid if >3cm, b/l, advanced, or distant mets. o Follicular Cancer- 15% of all thyroid cancers- avidly absorbs iodine. Worse prognosis than papillary cancer spreads via hematogenous route Hurthle Cell Cancer- more aggressive form that spreads by lymphatics and DOES NOT TAKE UP IODINE. Tx- Total thyroidectomy Tx- total thyroid with postop iodine ablation. o Medullary- 2-3% of all thyroid cancers. 1/3 sporadic, 1/3 familial, 1/3 MEN II Calcitonin. More malignant than follicular. Tx= total thyroid o Anaplastic- worst one. Seen in elderly. Prognosis in few months. Invades adjacent organs Chemo and radiation Pituitary Adenoma o Can be hyperperactive (Cushings, Galactorrhea, Acromegaly, hyperthyroid) or hypoactive leading to GH deficiency and hypogonadotropic hypogonadism o Dx- MRI or hormone levels o Tx- Transsphenoidal resection unless prolactin (medical management) HyperProlactinemia- inhibits GnRHdecreased estrogen/testosterone o Causes include prolactinoma, pregnancy, hypothyroid, psych medications, verapamil o Men get decreased libido and gonad size with galactorrhea and visual signs o Women- menstrual problems, dyspareunia, vaginal dryness. o Dx- high prolactin, MRI brain, TSH, pregnancy test o Tx- if not due to pregnancy or hypothyroid, give bromocriptine for 2 yrs. Acromegaly- broadening of skeleton from lots of GH AFTER epiphyseal closure. Causes big hands, feet, organs. Arthralgias, HCM and coarse facial features. HCM is the most common cause of death. o Results in DM and hyperhidrosis o Dx- IGF-1/Somatomedin C elevation. Glucose suppression test fails to suppress GH. o Tx- trans-sphenoid. Radiation for elevated lvls. Octreotide for GH suppression Craniopharyngioma- suprasellar tumor from Rathkes Pouch. 20-25% of pit lesions o Bitemp hemianop. Brain MRI is diagnostic. Tx- surgery. Can cause hyperprolactin, DI, or panhypopituitarism Diabetes Insipiduso Central- idiopathic, trauma or destructive process (Tb, sarcoid, tumor, syphilis) o Nephrogenic- hypoK, hypercal, lithium, demeclocycline, pyelo o HYPERNATREMIA MILD but polydipsia and polyuria common o Dx Low spec grav/low urine osmols in urine with 280-310 serum osmols. If serum osmols <280, most likely primary polydipsia Water deprivation test REQUIRED to make dx. ADH level low in central DI, normal in nephrogenic o Tx- Desmopressin for Central, Thiazide Diuretics for Nephrogenic SIADH-

Despite volume expansion, EDEMA IS NOT SEEN. Due to NATRIURESIS (which is due to ANP release, decreased proximal tubular sodium absorption (due to volume expansion) and RAAS inhibition) o Hyponatremia occurs and volume expansion occurs. o Can be caused by and lung pathology or CNS pathology or Tumors. o ACUTE hyponatremiabrain swellingseizure/coma/death o CHRONIC hyponatremiaasymptomatic or nausea/vomiting. Less commonly CNS symptoms. o Dx- water load test o Tx Asymptomatics: water restriction. Loop diuretic + NS. Lithium or demeclocycline Symptomatics- water restriction, NS or hypertonic saline. Hyponatremia pearls- Hypovolemic means volume contracted. Hypervolemic means volume expanded with edema. SIADH is WITHOUT edema Adrenal Insufficiencyo Primary (Addisons)- thought to be autoimmune but other primary causes include infectious disease (Tb, fungi, CMV, Toxo, Crypto and PCP) o Secondary- long term steroids cause this. The problem with this is that when patients are sick, they need EXTRA steroid replacement due to chronic suppression of ACTH. o Tertiary-hypothalamic disease o Clinical: weight loss, weakness, pigmentation, anorexia, nausea, postural HTN, abdominal pain Also lethargy/confusion, hypoglycemia, Low Aldo results in (onlyin primary adrenal insufficiency) Hyponatremia, hypoTN, decreased renal perufsion, weakness, shock , syncope, Hyperkalemia Adrenal Crisis- acute, severely symptomatic stage of adrenal insufficiency that can include severe hyponatremia and CV collapse with abdominal pain, AKI and death. Tx- fluids, hydrocortisone. o Dx- Decreased cortisol levels, increased plasma ACTH. ACTH test- give IV infusion of ACTHmeasure cortisolif no response can still be either primary or secondary. Must be repeated 4-5 days. If response after 4-5 days, then can diagnose SECONDARY insufficiency. This is a stupid method to me b/c you should jst measure ACTH to tell the difference btwn primary and secondary. o Tx- daily oral glucocorticoid and daily mineralocorticoid for primary. Secondary is tx with same thing but mineralocorticoids not necessary. Congenital Adrenal Hyperplasia- autosomal recessive due most often to 21-OHase deficiency. o Decreased cortisol/aldo production with increased ACTHadrenal hyperplasia with buildup of precursors leading to shunting to DHEA which causes virilization in females. o Salt wasting form of disease- emesis, dehydration, hypoTN, shock in first 2-4 wks of life. o Lack of aldo leads to hyponatremia and hyperkalemia. Lack of cortisol leads to hypoglycemia.

Dx- High levels of 17-OH Progesterone in serum Tx- medical replacement of cortical and aldo shuts off excess ACTH. Surgical correction of genital abnormalities Diabetes- Type I (5-10%, require insulin to live) and Type II (90%, norml to high insulin with resistqance, often diagnosed late.) o IGT- Fasting 110-126, OGTT 140-200 o In type I there are genetically susceptible individuals who usually have a trigger that sets off the autoimmunt rxn. No sx until 90% of cells are gone. o In type II, obesityFFA elevatedmuscles insulin resistantreduced glucose uptake. o Management A1C levels q3 mos with goals of <7%. Monitor daily levels at bedtime and before meals. Strongly encourage postprandial (90-120 mins too) Screen for microalbuminuria and BUN/Cr 1x/yr. Eye screening yearly, cholesterol yearly, foot care, BP q visit. o Hypertrigs with HDL depletion. o Screen adults q3 yrs starting at 45, or if family hx or other risks can start earlier. o Symptoms- polyuria, polydipsia, fatigue, weight loss, blurred vision, FUNGAL INFXN, Neuropathy Type I occurs over dayswks. Can present in acute DKA. Type II discovered on screening UA or blood sugar Complications: MI, stroke, claudication, impotence, neuropathy, proteinuria, retinopathy o Tx Insulin Intensive insulin tx- onlyin pregnants or in pts that are willing to monitor glucose many times daily. (.4-.5 per kg, with 40-50% basal and 50-60% pre-prandial) If unwilling to do intensive- 70%/30% NPH/Reg before breakfast and before evening meal for basal. And give regular for prandial control IF necessary. Sliding Scale- used in addition to intermediate insulin regimen. o Typical 150-200 2U. Increase by 50increase by 2U Decrease insulin 1-2 units per 20-30 mins physical activity. Must administer ALL insulin during illness. Surgery cases should get 1/3-1/2 usual daily insulin requirement. Type II Diabetics- diet and exerciseoral antihyperglycemics- start with metformin or sulfonylurea. Use combo tx if monotx fails. often progresses to need for insulin. o Complications- Macrovascular include high risk of atherosclerotic disease incl stroke, MI and PVD. Microvascular Nephropathy- KW nodular glomerular sclerosis due to hyaline deposition. OR. Diffuse Glomerular Sclerosis- hyaline deposition is GLOBAL.

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Microalbuminuria/Proteinuria- strict glycemic control necessary. Usually worsens. HTN develops during transition btwn microalbuminuria and proteinuria. 30-300 mg/day. o HTN worsens this. Initiate ACEIs IMMEDIATELY. o Once clinical proteinuria (dipstick) develops, glycemic control has NO benefit. Retinopathy- 75% after 20 yrs of diabetes. o Nonproliferative- hemorrhages, exudates, aneurysms. Usually ASYMPTOMATIC unless involves central macula Edema of macula is cause of visual loss. o Proliferative- new vessel formation. Leads to blingness due to either vitreal hemorrhage or retinal detachment Neuropathy- peripheral neuropathy (distal symmetrical) leading to stocking/glove pattern of lossulcerscharcots joints, allodynia (hypersensitivity to light touch) Mononeuropathies- secondary to nerve infarction. Autonomic Neuropathy- impotence, neurogenic bladder, gastroparesis, constipation Dawn Phenomenon and Somogyi Effecto Morning hyperglycemia o Dawn Phenomenon- due to increased nocturnal secretion of GH. o Somogyi Effect- rebound response to nocturnal hypoglycemia. o Distinguish btwn the two by taking a 3am sugar level. If low, this is Somogyi, if high it is probably dawn phenomenon (increase basal insulin) Glucagonom- necrotizing migratory erthema, glossitis, stomatitis, DM, hyperglycemia Somatostatinoma- malignancy tumor that presents with gallstones, diabetes and steatorrhea. VIPoma- rare pancreatic malignant tumor with watery diarrhea, achlorhydria, hyperglycemia and hypercalcemia

CNS/PNS Diseases: Strokeo Classes include TIA, reversible ischemic deficit (same as stroke but lasts longer than 24 hrs and resolves in <2 wks), Evolving Stroke and Completed Stroke. o TIA- lasts from few minutes to 24 hours. Reperfusion can occur either due to fibrinolysis or due to collaterals. Blockage does NOT cause permanent damage. Usually embolic but transient hypoTN can also cause this. High risk of stroke in subsequent months o Risk Factors- age and HTN. Other less impt ones smoking, DM, HLD, Afib, CAD, FHx, carotid bruit o Most common cause is heart embolization of thrombus from AFib. o Three important ones to remember: septic emboli from endocarditis, Afib embolus and ischemia due to atherosclerosis. o Thombotic Strokes- any of the arteries of the neck or brain vessels.

Lacunar Stroke- small vessel thrombotic dz, 20% of all strokes, affects subcortical structures (basal ganglia). HTN most impt risk factor. Occlusion due to vessel wall thickening NOT atherosclerosis. Healed strokes are called lacunae. o Classic Story of Thrombotic stroke- pt awakens from sleep with neuro deficits. o Embolic Stroke- rapid onset with maximal deficit. Contralateral hemiparesis/hemisensory loss, aphasia (if MCA) o Lacunar- focal, contralateral pure motor (Internal Capsule) or pure sensory (thalamus). o Dx- Non Con CT- ischemic (dark- but wont show up for 24-48 hrs) vs hemorrhagic (white). MRI more sensitive- and quicker. NOT first test, takes a long time EKG- AMI or AFib- for embolic stroke Carotid Duplex- for carotid stenosis MRA is DEFINITEIVE TEST for stenosis of vessels. o Tx- supportive (IVF, Airway, O2). tPA w/in 3 hours NOT if time is unknown or >3 hrs passed, or uncontrolled HTN, trauma, surgery, bleeding diathesis. MUST MONITOR FOR HMOERRHAGE- neuro checks, BP monitoring ASA if >3 hours. NO A/C have been proven effective. Hold Anti-HTNsive unless one of the following is present: BP >220/120 Significant reason for anti-HTNsive such as MI, dissection, heart failure. Thrombolytic therapy was given (decreased chance of hemorrhage) o Prevention- Depends on the cause: Atheroscleorsis of carotids- control HTN, DM, HLD, obesity, give ASA. Carotid Endarterectomy if >70% stenosis and symptomatic. Embolic dz- ASA Lacunar- control HTN Hemorrhagic Strokeo Intracerebral Hemorrhages (ICH) high mortality/morbidity. Hematoma formation/enlargement injury and increased ICP. Usually caused by HTN small rupture of vesselsmicroaneurysms. Amyloid Angiopathy, A/C Use, Brain Tumor, AVMs also cause ICH Usually loated in the basal gangliaponscerebellumelsewhere Clinical- focal neurologic deficit worsening over 30-90 mins- eventually can lead to h/avomitingstuporcomadeath Dx- CT Tx- ICU admission, ABCs, BP Reduction (GRADUAL) with nitroprusside only if >180/105. Mannitol and diuretics to decrease ICP. IF CEREBELLARsurgical evacuation. o Subarachnoid- usually saccular aneurysms at circle of willis bifurcations. Three causes- trauma, ruptured aneurysm and AVM

Sudden, severe worst h/a of life. Sudden loss of consciouness, vomiting, meningeal irritation. Retinal Hemorrhages (MUST MUST DO OPHTHO EXAM TO RULE THESE OUT AND RULE OUT PAPILLEDEMA). Dx- noncon CT- which can be negative in up to 10%. LP if CT is nondiagnostic (xanthocrhomia and RBCs). Once diagnosed- get cerebral angiogram for site of bleeding so you can clip that shit. Complications- re-rupture in up to 30%, vasospasm in 50%, seizures, communicating hydrocephalus, SIADH Tx- Surgical (berry aneurysms). Medical- reduces risk of rebleeding with bed rest in dark room, sttol softeners to avoid straining (increasing ICP), Analgesia, IVF, Control HTN (SLOWLY!!!!!), CCBs for vasospasm. Parkinsons Diseaseo Loss of dopamine neurons in the substantia nigra and locus ceruleus (midbrain). o Shy-Drager Syndrome- parkinsonian sx + autonomic insufficiency o Clinical: Pill rolling tremor, bradykinesia, rigidity, poor postural reflexes (shuffling gait, turning on end, stooped posture), masked facies, impaired cognition, apathetic, progressive. o Medications that can cause it: schizo drugs, metoclopromide, reserpine o Tx- No cure- goals to delay progression. Carbidopa/Levodopa (Sinemet)- Side Effects- dyskinesia (involuntary movements), N/V, anorexia, HTN, hallucinations Levodopa has on-off phenomenon during tx leading to fluctuations in symptoms throughout day. Dopamine Agonists (bromocriptine, pergolide, pramipexole) Delays need for levodopa early on. Useful for sudden episodes of hesitancy/immobility. Selegiline- MAO-B inhibitor. Adjunct used early on. Amantadine- increases endogenous dopamine but only transiently improves sx Anticholinergics- Benztropine. USEFUL FOR PATIENTS WITH TREMOR Surgery (deep brain stimulation)- if pt doesnt respond to meds o Difference btwn Progressive Supranuclear palsy and Parkinsons: PSP does not cause tremor, but causes ophthalmoplegia. Huntingtons Choreao Chorea, personality changes, impaired mentation (progressive dementia), Unsteady gait, Incontinence o MRI shows atrophy of caudate. Tx is symptomatic though dopamine blockers may help chorea and psychosis. Tremoro Physiologic Tremor- caused by fear/anxiety, hypoglycemia, hyperthyroid, pheo, or withdrawal. Tx- underlying cause, which if unknown, none necessary. o Essential Tremor- AD inheritance induced by intentional activity (drinking, using utensils) DECREASED BY ALCOHOL USE. Tx= Propranolol Ataxia- Gait instability, loss of balance and impaired coordination all caused by either alcohol intox, B12/thiamine def, cerebellar problems MS, syphilis,

Friedrichs Ataxia- AR inheritance onset by young adulthodd. In addition to ataxia, one experiences nystagmus, impaired vibratory sense and proprioception. o Ataxia-Telangiectasia- AR inheritance, onset in childhood. Friedrichs + telangiectasias. Increased cancer incidence. o Tx- underlying cause Tourettes Syndrome- OCD assoc. Onset b4 21 yrs old. AD inheritence. o Motor or phonic tics. o Tx- clonidine, pimozide, haldol Dementia- Things you dont already know o Binswangers Dz- insidious onset due to diffuse subcortical white matter degeneration seen in pts with long-standing HTN and atherosclerosis. o Picks Dz- clinically identical to Alzheimers o Pseudodementia- severe depression causes decline in cognition difficult to distinguish from Alzheimers. Responsive to antidepressants. Alzheimers Dzo Risks include family hx or Downs Syndrome. Chromosomes 14,19, 21. o Pathology is senile plaques (neuritic processes surrounding central amyloid core) with neurofibrillary tangles (neurofilaments in cytoplasm of neurons. o Clinical Features- insidious onset with steady progression. Avg time to death is 5-10 yrs. Early-forgetfulness, impaired ability to learn new material, poor concentration Intermediate- impaired memory, awareness but denial present, Visuospacial disturbances (getting lost in familiar places). Late- ADLs need assistance. Paranoid delusions and hallucinations common. Cant remember family members names. Death is usually secondary to infection due to eventual debilitation. o Dx- Clinical dx. CT scan or MRI shoes diffuse cortical atrophy with enlarged ventricles. o Tx- AchE inhibitors- Donepizil. Tacrine is used sometimes but its worse due to 4x/daily dosing. Dementia with Lewy Bodies- Alzheimers + Parkinsons with more rapid progression than Alzheimers. Visual hallucinations predominate with some extrapyramidal features and fluctuant mental status. Sensitive to adverse effects of neuroleptics. Tx is with alzheimers drugs but also with neuroleptics. Delirium o Medical disturbance or condition resulting in RAPID cognitive dysfxn, disorientation, perception abnormalities (hallucinations), slow-blunted response o PDIMMWIT- Postop state, dehydration, infection, meds, metals, withdrawal, infammation, trauma o Dx- MMSE, Labs (chem, B12, thiamine), LP unless contraindications o Tx- Haldol, Supportive, Underlying cause Coma- depressed level of consciousness with 0 response to any stimuli caused by b/l structural brain lesions, global brain dysfunction, Psychiatric causes (conversion, malingering) o Abnormal pupil reflex- intracranial structural lesion or drugs that affect pupil.

Bilateral fixed, dilared pupils= SEVERE ANOXIA Unilateral Fixed Dilated Pupil- CN III compression with herniation Approach to a patient with coma- vitals/ABCs, stabilize C Spine, do GCS. Do a motor exam (mass lesion if assymetrical, metabolic/toxic if symmetrical) Brainstem Reflexes- papillary light reflex- see above. Dolls eyes, breathing. Labs, Tox screen, CT/MRI spine, LP for meningitis or SAH o Tx- underlying cause. Airway control with o2, nalocone, D50, thiamine (BEFORE D50), Lower the intracranial pressure. Locked in Syndrome- caused by infarction of VENTRAL PONS Brain Herniation- Brain tissue moves past anatomic barriers due to mass lesion or edema. o Uncal Herniation (transtentorial)- compression of midbrain leading to CN III ipsilateral anioscoria with sluggish papillary reflex. Contralateral hemiparesis Progressive brainstem progression o Tonsillar Herniation- medial portions of cerebellar hemispheres compress medulla through foramen magnum. Compression of vital cardiorespiratory centers. o Central Herniation- supratentoral lesions. Change in mental status, midpoint small pupils, posturing of extremities, cheyne stokes breathing, hyperventilation. Incresed muscle tone and bilateral + Babinskis o Dx- CT Scan o Tx- intubation, neurosurgery, Lower ICP Multiple Sclerosis- CNS demyelination diz throughout white matter (plaques). CLASSIC LOCATION OF PLAQUES IS LATERAL VENTRICULAR ANGLES o Pyramidal (weakness/spasticityhemiparesis) and Cerebellar (ataxia, intention tremor) pathways, MLF (Internuclear Ophthalmoplegia- ipsilateral medial rectus palsy and contralateral horizontal nystagmus), optic nerve (transient visual disturbances due to optic neuritis (monocular visual loss w/ pain on movement of eyes, central scotoma and decreased papillary rxn)) and posterior columns (transient sensory defects- most common presenting symptom) are the most commonly involved tracts, which helps you to come up with symptoms. o Incidence higher at higher latitudes and in women. o Other symptoms include- Loss of bladder control (UMN lesion), Impotence (autonomic), Neuropathic Pain (hyperesthesias and Tic Doureaux) o Dx- Two episodes of sx, with two white matter lesions on imaging (or one white matter lesion + abnormal oligoclonal bands in CSF). Three most important tests to get: LP, MRI and Evoked Potentials. o Course- 20s-30s w/ optic neuritis, numbness or weakness. Most cases of MS are clinically silent Relapsing Remitting- self-explanatory Secondary Progressive- Pts with relapsing/remittinggradual worsening of sx until progressive loss later in life.

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Primary Progressive- steady progressive disease tends to have less visual but more of the other symptoms involved. o Usually attacks occur 1x/yr and last >24 hrs. o Tx is symptomatic. There is no cure. Acute attacks- High Dose IV Steroids. Usually resolve w/ or w/out tx in 6 weeks. If refractory, therapeutic plasma exchange. Disease Modifying Therapy- IFN + glatiramir acetate of which only short studies have been done, so long term benefits unknown. If RAPIDLY progressive- give cyclophosphamide. Guillain Barre Syndrome- polyneuropathy affecting motor nerves preceded by a viral/ mycoplasmal URI. Also seen is Campylobacter, CMV, Hepatitis or HIV. o ASCENDING weakness of all four extremitiesrespiratory, facial and bulbar (swallowing) muscles. o Usually symmetric. Sensory loss not typical. But can be painful. o If autonomic involvement: dangerous complications- arrhythmias, tachy o Signs of recovery in 1-3 wks is good prognosis. If >6 wks, then relapsing syndrome is likely. o Dx- CSF shows elevated protein (Igs) with a NORMAL cell count. Nerve conduction velocities could be decreased. o Tx- monitor pulm fxn with possible mechanical ventilation. IVIG for significant weaknessPlasmapheresis. Do NOT give steroids. CNS Neoplasms- most commonly mets but common primaries are gliomas meningiomas. o Increased ICP (hydrocephalus + mass effect) headaches, N/V (all on awakening), Reduced consciousness, Papilledema and Herniation. o Focal Deficits seizures, cranial nerve deficits (mass effect), hyperfunctioning tumor causing overproduction of a hormone or of CSF (if choroid plexus) o Dx- MRI W/ AND W/OUT GADOLINIUM. Brain Biopsy if still suspected (for type) o Tx- Resect a meningioma, pituitary adenoma or schwannoma. Gliomas get radiation (others get radiation postsurgically). Always control Increased ICP with mannitol, diuretics, hyperventilation and STEROIDS Astrocytoma- 80% of all CNS tumors o Infiltrate brain and have indistinct boundaries o Spread along White matter tracts- can cross corpus callosum o Cure is rare, recurrence is high. Oligodendrogliomas- 40-50 yo with malignant but indolent progression. Survival-10-15 yrs Primary Lymphomas- immunosuppressed with <2 yr survival. Metastatic- LungBreastskinKidneyGI Meningiomas- 40-50 yo women, attaches to dura and is a round mass with welldefined dural base compressing underlying brain causing focal issues. Potential for surgical cure but high rate of recurrence. Schwannomas- benign, unilateral at the cerebellopontine angle8th CNgrows to affect 5th CN and 7th CN. Hearing loss is first symptom with tinnitus, nystagmus and loss of balance. Tx= surgery Secondary insults that can contribute to Traumatic Brain Injury:

Hypercapniavasodilation (exacerbating problem of already increased IV volume in the cranium) Key features of Traumatic Brain Injuryo Elevated ICP >20 mm (nml 5-15) is worrisome due to decreased cerebral perfusion pressure (MAP-ICP must be >50)loss of autoregulationvasodilation vasogenic edemaworsening ICP. Transtentorial herniation can occur leading to bilateral fixed and dilated pupils due to CN III compression. Basilar Skull Fx- raccoons, battles, hemotympanum, oto/rhinorrhea o Coup Injury- injury at site of impact o Contrecoup Injury- injury OPPOSITE site of impact Diffuse Axonal Injury- global damage with severe neurologic dysfxn, CT scan usually does not show elevated ICP but shows punctate hermorrhages in tracts. Mortality 33% Treatments to lower ICP: reverse trendelenburg, hyperventilation (decreased CO2 causes vasoconstriction), Mannitol, diuretics, narcotics for sedation, hypothermia Epidural Hematoma- middle meningeal artery- brief loss of consciousness, lucid interval, coma due to transtentorial hernation compressing midbrain. Dx= CT Tx= Decompression Subdural- venous bleeding after blunt heads trauma- due to venous bleeds (bridging veins) o Risk factors include brain atrophy, anticoagulation. o 2x as common as epidural. o Same symptoms as epidural except patients are MUCH sicker. Poor Prognosis. o Tx for acute is surgical evacuation. Chronic may resolve spontaneously. o Dx- CT Concussion- brain injury following blunt traumabrief loss of consciousness. o EP dysfxn of MIDBRAIN secondary to impact leading to dizziness, loc, delay in answering questions. May have headache, irritability or amnesia. o If you have vomiting, delirium or focal neuro deficit must r/o hematoma (signs of increased ICP). Myasthenia Gravis you know the clinical presentation. Due to acetylcholine nicotinic antibodies. Dx= acetylcholine receptor antibody is test of choice. EMG shows decremental response with repetitive stimulation. CT to r/p thymoma. EDROPHONIUM TEST. o Tx- Pyridostigmine- sx benefit. Thymectomy (even in absence of thymoma). Steroids, Azathioprine if pyridostigmine fails.. Plasmapheresis if pt in resp failure and all else fails. Monitor FVCs and have a LOW THRESHOLD FOR INTUBATION (1L FVC) Duchennes- X-linked recessive mutation of dystrophin. No infglammation. o Progressive, symmetric weakness that starts in childhood. Proximal muscles. o Eventually involves the respiratory muscles. GOWERs + o Calf pseudohypertrophy. Wheelchair boundresp failuredeath in 3rd decade o Dx- Serium CPK followed by DNA TESTING rather than biopsy. o Tx- none but can try prednisone. Can do surgery for progressive scoliosis. NFT I- AD with caf au lait, neurofibromas, glioma/meningioma, axillary freckling, Lisch Nodules. o Complications-scoliosis, pheo, optic nerve glioma, Renal Art stenosis, seizures

NFT II- AD and include bilateral acoustic neuromas, multiple meningiomas, cataracts. Tuberous Sclerosis- AD with cognitive impairment, epilepsy, facial angiofibromas, Adenoma Sebaceum. o Retinal hamartomas, renal angiomyolipomas, cardiac rhabdomyoma. Sturge Weber- acquired disease with capillary angiomatosis of pia mater. Facial vesicular nevi (port wine). Epilepsy and Mental retardation are common. Von-Hippel Lindau- AD with cavernous hemangioma of the brain/brainstem, renal angiomas, cysts. Assoc with RCC. Syringomyelia- abnormal collection of fluid in spinal cord parenchyma due to cranial base malformation, intramedullary tumors or traumatic spinal cord necrosis. o Capelike distribution of loss of pain and temp. o Dx- MRI Tx- synringosubarachnoid shunt Brown-Sequard- hemisection of cord leading to contralateral loss of pain/temp and ipsilteral loss of position/vibration Transverse Myelitis- Occurs AFTER VIRAL INFXN with RAPID course. Lower extremity weakness/plegia, back pain, sensory deficit. o Urinary retention common o MRI with contrast and High dose steroids. Unpredictable prognosis Polio- anterior horn and motor neurons of spinal cord and brainstem causing LMN signs- asymmetric muscle weakness, absent DTRs, flaccid muscles. NORMAL SENSATION o No tx but yes vaccine Dizziness- presyncope, vertigo, cerebellar, psych. o Dx- audiogram if vestibular suspected, CT/MRA if suspecting TIAs, MRI of post fossa if mass lesion suspected o Tx- underlying cause Vertigo: o Central: gradual onset, mild intensity with other brainstem findings (dysphagia, dysarthria, diplopia)- due to CVA/Tumor- worse than peripheral Multiple Sclerosis, Vertebrobasilar insufficiency or migraine associated o Peripheral: cochlear or retrocochlear causing abrupt onset N/V, with head positioning being impt to control sx Benign Positional Vertigo- only in specific positions and lasts only a few moments. Abrupt onset. >60 yo. After head injury. Recovery in <6 mos Menieres Disease- tinnitus, vertigo, hearing loss Acute Labyrinthitis- viral infxn of cochlea. Lasts days Ototoxic drugs or Acoustic Neuromas Vasovagal Syncope- Dx- tilt table. Tx- Beta Blockers, elevate legs Tx Orthostasis with increased sodium and water intake. Consider fludrocortisones. Also can expect a positive tilt-table test with this one, and along with vasovagal is associated with premonitory sx such as lightheadedness and nausea. Seizures- abnormal discharge of brain wave activity. Epilepsy means recurrent idiopathic seizures. o Causes (4 Ms, 4 Is) Metabolic, Masses, Missing Drugs (antiepileptic noncompliance or withdrawal from alcohol etc), Miscellaneous (pseudoseizures-

Types Partial- begins in one part of brain and produces focal symptoms. Simple Partial- Consciousness remains intact Complex Partial- consciousness impaired with postictal confusion. Automatisms, aggressiveness, Olfactory OR gustatory sensations Generalized- LoC Tonic Clonic- b/l symmetric, no focal onset. o Fall to groundtonic phase (rigidity)Clonic phase (jerking limbs for at least 30 secs)Flaccidity Comatose Regain consciousness Postictal confusion o Tongue biting, apnea, vomiting, incontinence common Absence- 100x/daily sometimes. Very brief. o LoC but no loss of posture. Eyes blink/Head nods o Dx- check anticonvulsant levels to make sure they are therapeutic. Serum Na, Ca, Glucose, BUN EEG- abnormality is NOT adequate to dx seizure. CT Scan- structural lesion. LP and cultures- if febrile o Tx- ABCs (especially for aspiration) If hx of seizure- check compliance w/ therapy. Manage by neuro for epileptic drug regimens. 70% controlled on one drug. Additional 20% controlled on multi drug regimen If seizures persist, increase dose of drug 1 until toxicity appears then add a second drug Continue drug regimen that controls seizures for 2 yrs then slowly taper. First Seizure- EEG and neuro consultanticonvulsant tx Stats Epilepticus- IV diazepam, IV phenytoin, IV dextrose. Give phenobarb if doesnt respond to these. ALS- UPPER and LOWER motor signs due to anterior horn cells and corticospinal tracts. o 50-70yo, 10% familial. 80% mortality at 5 yrs. o Clinical- PROGRESSIVE MUSCLE WEAKNESS with atrophy (arms/legs first), no pain. Muscle Cramps, spasticity, Fasciculations Impaired bulbar musclesdysphagiaaspiration End Stage ALS is respiratory failure. Unaffected: bowel/bladder, sensation, cognition, EOM o Dx- EMG/NERVE CONDUCTION- confirms lower motor neuron lesions and rules out NMJ disorders. Involvement- bulbar, cervical, thoracic, lumbosacral o Tx- supportive. Riluzole- glutamate blocking agent delays death by 3-5 mos o

psychiatric in origin with normal EEG, Eclampsia, HTNsive encephalopathy). Intoxications, Infections, Ischemia, Increaed ICP

DDx for Bells Palsy- Trauma, Lyme, Tumor (acoustic neuroma), Guillain Barre (b/l), Herpes Zoster o Dx- Clinicalb but consider Lyme in endemic areas o Tx- Resolution in 1 month. Short course of prednisone and acyclovir if necessary. Wear eye patch at night to prevent corneal abrasion.

Connective Tissue And Joint Diseases: o SLE- autoimmune disorder leading to inflammation and tissue damage in multiple organ systems. African American Women of childbearing age. o Due to autoantibody productionimmune complexescomplement activation destruction of tissues/vasculitis o Neonatal Lupus- Skin lesions, Cardiac abnormalities (AV block, transposition, Valvular and septal defects). Seen in mothers with ANA NEGATIVE LUPUS but Ro Positive. o Clinical: Immunologic- Anti Sm, Anti dsDNA, impaired immune response. Malar rash Discoid rash ANA Mucocutaneous ulcers Neurologic sequelae- seizures, psychosis, depression, H/A, TIA, CVA Serositis Hematologic abnormalities- hemolytic anemia, leucopenia, TCP Arthritis Renal disease- proteinuria >0.5g/day, hematuria, casts, azotemia, GN Photosensitivity Constitutional symptoms- fatigue, malaise, weight loss Cardiac- Myocarditis or Libman Sacks Endocarditis- anticoagulate GI- nausea/vomiting, dysphagia, PUD o Dx- Positive ANA with confirmatory anti-Sm and anti-dsDNA. Anti-histone- drug induced SLE (does not affect kidneys or CNS)hydralazine, procainamide, ING, chlorpromazine, methyldopa, quinidine Ro and La- Sjogrens, Neonatal lupus (see above), C2, C4 deficiencies Complement decreased. Anti cardiolipin and Lupus Anticoagulant Anti-Phospholipid- recurrent venous thrombosis (PE), recurrent fetal loss, TCP, Livedo Reticularis. Prolonged PT and aPTT that is NOT corrected by adding serum o Tx- long term A/C o Tx- avoid sun exposure, NSAIDs for the less severe sx. Systemic steroids for acute exacerbation or severe manifestations, Hydroxychloroquine for constitutional, cutaneous, articular manifestations. Cyclophosphamide for renal. o Scleroderma- chronic connective tissue disease leading to widespread fibrosis due to collagen deposition.

Diffuse- widespread skin involvement, rapid onset after Raynauds starts, visceral involvement including lungs, heart, GI and kidneys. ANA but lacks antiCentromere. Poor prognosis. Interstitial lung dz common. o Limited- CREST- calcinosis of digits, Raynauds, Esophageal dysmotility, Scelrodactyly, Telangiectasias. Skin invovlemnt only distal extremities. Delayed onset after Raynauds starts. ANTI CENTROMERE o Clinical: Raynauds appears first (can lead to digital ischemia or ulceration). Cold temp/stress cause color changes- blanching, then cyanoticred Cutaneous Fibrosis- sclerodactyly GI Involvement- most pts. Dysphagia/reflux, delayed gastric emptying, constipation, distention. Pulm Involvement- MOST COMMON CAUSE OF DEATH FROM SCLERODERMA. Cardiac- pericardial effusions, myocardialCHF/arrhythmia Renal- renal crisismalignant HTN in pts with diffuse scleroderma o Dx- AntiCentromere in limited, Anti-Topoisomerase I in diffuse. Barium swallow and PFTs to detect complications o Tx- None. NSAIDs for pain H2 blockers for reflux Avoid cold/smoking for Raynauds- can also use calcium channel blockers. Sjogrens- autoimmune disease seen in women in which lymphocytes destroy salivary and lacrimal glands, but can also involve, skin, lungs, thyroid, liver o Primary- dry eyes and mouth with lymphocytic infiltration of minor salivary glands (on histology). NO other rheumatologic disease o Secondary- dry eyes/mouth and ANOTHER connective tissue disease. o Clinical: Dry eyes/mouth, arthritis/algias, Interstitial nephritis or vasculitis o Dx- ANA + , Ro, La +, o Tx- pilocarpine (enhances secretions), artificial tears, oral hygiene, NSAIDs, steroids for arthritis Rheumatoid Arthritiso Variants Feltys- anemia, neutropenia, splenomegaly and RA Stills before 18 yrs old. Extra-Articular sx *see below* predominate o Inflammatory autoimmune dz involving synovium, which, when inflamed, causes damage to cartilage and bone. o 20-40 yo in women. o Clinical: Symmetrical Polyarthritis involving every joint in the body EXCEPT the DIPs. 4 out of 7 Criteria: Morning Stiffness x 6 wks 3 or more joint arthritis x 6 wks Symmetric arthritis x 6 wks Hand joint arthritis x 6 wks

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RF Rheumatoid Nodules Radiographic RA changes (erosions & periarticular calcifications) Constitutional symptoms should be present (morning stiffness esp) but also low grade fever, weight loss. Hand Deformities including Swan Neck, Ulnar Deviation, Boutenniere C-Spine involvement- LIFE THREATENING COMPLICATION OF RA is SUBLUXATION OF C1-C2. Cardiac- pericarditis, pericardial rffusion, valve insufficiency. Pulm- pleural effusions, interstitial fibrosis Ocular- episcleritis or scleritis Soft Tissue Swellings Sjogrens Xerostomia Rheumatoid Nodules (extensor surfaces) can also be in lungs, pleura or pericardium) Dx- RF titers correlated with severeity of disease. Anemia of chronic disease present. Tx- prevent/halt destruction. Do exercise along with pharmacological tx Symptomatic- NSAIDs for pain Steroids if NSAIDs dont work, but make them short term and low dose. DMARDs- page 248