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

demand exceeds supplyo Risk Factors: DM, HTN, HLD, Cigs, Age (M>45, F>55), FHx, high Homocysteineo 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 ACEI’s/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 vesselo 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:

o Positive Stress Testo Angina +

Noninvasive tests are nondiagnostic Persistent despite optimal medical therapy Occurs after recent MI

o Severely symptomatic with urgent diagnosis neededo Evaluation of valvular disease-o 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. CABG-

o 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 MIo 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 (Prinzmetal’s Angina)

o Transient coronary vasospasm which many times has a fixed atherosclerotic lesion.

o Occurs AT REST. Usually associated with a VENTIRCULAR ARRHYTHMIAo ST-Elevation on EKG during chest pain (TRANSMURAL ischemia)o 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 hrso Falsely elevated in patients with renal failure

Thrombolytic Therapy- should happen within 6 hours but is OK up to 24o Indications include STEMI refractory to nitroglycerine. tPA is first choiceo Contraindications- >180/110 BP, Trauma, PUD, Stroke, Invasive Procedure,

Aortic Dissection Diagnosis of MI: Treatment of MI-

o Tele, IV access, supplemental O2 and analgesics (nitrates, morphine)o ASA, Beta Blockers, ACEIs, Statins- all long term medications that should be

startedo Oxygen can help to limit myocardial injuryo Nitrates decrease preload (demand) and decrease afterload. Dilate coronary

arteries also (increases supply)o Morphine- for analgesiao Heparin- LMWH is better

Complications of Acute MI-o 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 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 suspected- tx= 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 Dressler’s 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 Dissectiono Pulmonary: PE, pneumothorax, pleuritis, pneumonia, asthmao GI- GERD, Esophageal spasm, PUD, rupture of esophaguso Chest Wall- costochondritis, muscle strain, rib fracture, herpes zostero Psychiatric- panic/anxiety attacks

CHF- an inability of the heart to meet the body’s circulatory demands o SHOULD DO:

CXR for pulm edema, caediomegaly

EKG Enzymes to ROMI CBC (anemia) Echo (EF, pericardial effusion)

o 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.

o High Output Heart Failure- INCREASE in ouput needed for requirements of peripheral tissues to be met

Anemia, Pregnancy, Hyperthyroid, AV Fistula, Paget’s Dz of bone, Mitral Regurg, Aortic Regurg

o Systolic Failure- impaired contractility leading to low EF. Causes include recent MI, CM, or myocarditis.

o 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)

o 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

o 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

o Diagnosis:

o 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)

EKG—nonspecific but can show hypertrophy or enlargement MUGA Scan- RBCs tagged with technetium 99 and imaged during

stress. Gives precise WMA’s and EF’s. 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 Complexes-o Early beat in atria which can be due to excess adrenergic stim, drugs, alcohol,

tobacco, ischemia, electrolytes, infectiono 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 ventricleo Causes- hypoxia, electrolyte abnormalities, stimulants, caffeine, medso SLOWER than normal conduction and therefore, WIDE QRSo 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-o 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 cardioversiono 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

o 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

o 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/

symptomatico 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

o 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 sotalolo 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 doesn’t work.

o 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.o Long term defibrillator

Bradyarrhythmias-o Sinus Brady- <60 bpm- doesn’t 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 doesn’t help

pacemakero Sick Sinus Syndrome-Persistent, spontaneous sinus bradycardia causing

dizziness, confusion, syncope, fatigue, CHF. Pacemaker which causes pacemaker rhythm- spike on EKG-

Indications-o Symptomatic Heart Block or Bradyarrhythmiao 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 doesn’t conduct- block at AV node. NO TREATMENT

Mobitz II- NO prolongationjust dropped QRSo 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 usuallyo 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 regurgo Dx- EKG/Echo/CXR consistent with CHFo 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.o 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 Echoo 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 doesn’t 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, deatho Dx-ESR AND ELEVATED ENZYMESo Tx- supportive and tx underlying causes

Pericardial Diseases-o Acute Pericarditis-

Causes: postviral (most common- preceded by flulike illness such as

Coxsackie, HIV, hepatitis), bacterial (Tb), fungal

Acute MI- 24 hrs later (or Dressler’s- 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 don’t 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 Syndromeo Clinical: Muffled heart sounds, soft PMI, dullness at left lung base, Friction rub

MAY OR MAY NOT BE PRESENTo 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.

o 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 soundso 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 wouldn’t 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 Stenosis-

o 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 Anginao Caused by calcified bicuspid or tricuspid, congenital unileaflet valve, rheumatic

fevero 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, Marfan’s, 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, Corrigan’s Pulse (water hammer pulse at radial artery), De Musset’s 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 Regurg- o 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 ruptureo 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, Marfan’s or Cardiomyopathy

o Clinical that you don’t already assume: Holosustolic murmur at apex radiating to back or clavicle AFIB IS COMMON Loud P2, S3 gallop

o Dx- Echoo 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), Ebstein’s anomaly (Lithium), Carcinoid, SLE

o Clinical you don’t 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 pressureo 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 Ehler’s Danlos/Marfan’s/Osteogenesis imperfecta.o VERY rarely sudden death, rarely Mitral Regurg resultso Clinical you don’t 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- echoo Tx- If murmur, then must give Abx ppx. Beta Blockers for CP (if present)

Rheumatic Heart Disease-o Mitral Stenosis due to GAS infxn due to immune mediated damage to valveso 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, ASLOo Tx- Penicillin/Erythromycin for pharyngitis.

ACUTE RF is managed with NSAIDS PPx for dental procedures

Infective Endocardtitis- usually involves valvular cuspso 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- Duke’s 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 embolizeo 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, fatigueo 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 HTNEisenmenger’s/ RV failure

AFibpossible strokeo 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 don’t 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- ECHOo Complications- Endocarditis, Aortic Regurg, CHF, Einsenmenger’so Tx- Endocarditis PP. Surgery only when pulm blood flow:systemic blood flow

ratio is >1.5:1 Coarctation of the Aorta-

o Narrowing/constriction of aorta at origin of L subclavian usually. Leads to increaseds LV afterload.

o HTN in upper extremities with hypoTN in lower extremitieso Mid-diastolic murmur over backo Symptoms: headache, cold extremities, claudication, leg fatigueo Dx- EKG shows LVH and CXR shows notching of ribso Complications- HTN, Berry aneurysm, Infective endocarditis, Dissectiono 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 PREEMIESo 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

o Dx- CXR shows increased pulm markings, dilated pulm artery, enlarged hearto 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 damage-

IMMEDIATE 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 causeTraumaMarfan’s/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

Causes include HTN, trauma, smoking, vasculitis, Syphilis/Marfan’s(thoracic)

o Clinical you don’t already know- mostly asymptomatic Throbbing pain in hypogastrium Expansion and rupture indicated by sudden, severe pain OR:

Grey Turners Sign- ecchymosis on the flanks Cullen’s Sign- ecchymosis around the belly button.

TRIAD:ABDOMINAL PAIN, HYPOTN, PALPABLE PULSATILE MASS- RUPTURE!!!!

CV Collapse, syncopeo Dx- U/S for location AND size of AAA. CT in hemodynamically stableo Tx-

Unruptured- If >5cm resection recommended, If <5cm it is controversial Ruptured- Surgery

Leriche’s Syndrome- atheromatous Occlusion of distal aortabilateral claudication, impotence and absent femoral pulses.

PVD- usually coexisting CAD, diabetes, smoking, HLD, HTN, hyperhomocystinemiao Most common sites of occlusion include Hunter’s Canal (Sup. Femoral Art),

Popliteal, Aortoiliaco 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 P’s Pallor, Pulselessness, Paresthesias, Paralysis, Poikilothermia, Paino 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 ANKLEo 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 ulcerso 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 doesn’t 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 cordo 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. Tx- surgery

PULMONARY DISEASES: COPD-

o 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 beta2’s.

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

Asthma-o Airway inflammation and hyperresponsiveness that is reversibly obstructiveo Can begin at ANY AGE!o Extrinsic- atopic patient with IgE to environmental triggers. Assoc with hay

fever/eczemao Intrinsic- not assoc with atopy or triggerso Tachypnea, diaphoresis, wheezing, accessory muscles, chest tightnesso Sign of impending doom- Paradoxical movement of abdomen and diaphragmo Sx worse at nighto 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 mechanismso Cause identified in < half patients. Less common today due to modern

antibioticso Causes- CF, Infection, airway obstructiono Clinical Features- chronic cough with large amounts of mucopurulent, foul-

smelling sputum. Dyspnea, hemoptysis, recurrent/persistent pneumoniaso 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 complicationso 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 SMOKINGo Asbestos- shipbuilders, construction, mechanics, painting. Synergistic with

smokingo Radon- common in basementso 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 Horner’s Syndrome- invasion of sympathetic chain by an apical

tumor Pancoast Tumor- superior sulcus, usually squamous cell tumor-

apical tumor involving C8 and T1-T2 causing shoulder pain radiating down arm.

o Upper extremity weakness, pain, Horner’s 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 Clubbingo 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), 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. o Tx-

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 Masses-o Mestastatic Cancer is the most common cause of mediastinal mass in elderlyo Anterior-thymus, thyroid, lymphoma, teratomao Middle- lung, lymphoma, aneurysms, cystso 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, Horner’s, phrenic

o Dx- Chest CT (which, if suggestive of benign mass, and asymptomatic pt, can follow)

Pleural Diseases-o 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 C’s: 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- o uncomplicated gets antibioticso Complicated/ Empyema gets chest tube drainage with

injection of thrombolytic agentso 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

traumatico 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, CPRo 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 diagnosiso Classification-

Environmental- asbestos, silicosis, berylliosis, coal worker’s 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 pneumonitiso Symptoms- Dyspnea, cough, fatigue, bibasilar rales, DIGITAL CLUBBING, pulm

HTNo 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- Bell’s 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 cigso Dyspnea and dry cough (again…oy)o Other complications: spontaneous pneumothorax, lytic bone lesions, diabetes

insipiduso CXR is honeycombing and CT shows cystic lesionso Prognosis variable. Tx- corticosteroids or lung transplant

Wegener’s Granulomatosis-o Necrotizing granulomatous vasculitis- vessels of lungs, kidneys, upper airway.

URI/LRI, Glomerulonephritis, pulmonary nodules are commonplaceo Dx- Tissue bx is gold standard but C-ANCA shows high sensitivityo Tx- steroids and immunosuppressives

Churg-Strauss- Systemic vasculitis- Granulomatous dz seen in patients with asthmao Pulmonary infiltrates, rash and eosinophilia due to skin, muscle and nerve

lesions o Dx- Eosinophilia and P-ANCAo Tx- steroids

Coal Worker’s Pneumoconiosis-o Accumulation of dust in the lung’s and tissue’s reaction to its presenceo Simple- causes no disabilityo 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 exposureo Bronchogenic carcinoma (smoking synergistic) and mesotheliomao CXR shows hazy infiltrates and b/l linear opacities along with Pleural Plaqueso NO TREATMENT

Silicosis- LOCALIZED and NODULAR peribronchial fibrosis (in the UPPER LOBES)o Can be acute after massive exposuredeath or chronic- years aftero Increased risk of Tb if chronic o Mining, Stone cutting, Glass manufacturingo 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 testo Tx- glucocorticoids

Hypersensitivity Pneumonitis- inhalation of antigens to alveolichronically leads to restrictive lung dz.

o Serum IgG and IgA to inhaled antigen is commono Acutely develops flu like picture with Pulmonayr infiltrates on CXRo 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 & steroidso 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 yrso CXR shows ground glass or honeycombingo Definitive dx is by biopsy but even this may yield nonspecific findingso 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 +/- cougho Signs include tachypnea, tachycardia, cyanosisand

impaired mentation. Diagnosis:

ABGo Hypoxemia- either V/Q, shunt or hypovent

Hypercapnia- always hypovent Tx- underlying disorder- bronchodilators, steroids, abx

Supplemental oxygen if hypoxemico Hypoxic Failure: Lowest concentration that provides

sufficient oxygenation to avoid toxicityo 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 breathingo Increased dead space due to obstruction and dectruction of pulm cap bedo Low FVC low FRCo Causes- sepsis, aspiration, trauma, pancreatitis, drug OD, Intracranial HTN, o 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 Ventilation- o Goals: maintain alveolar ventilation and correct hypoxemiao 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 patient’s 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 patient’s 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). 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 exerciseo 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 HTN-o Dx of exclusion due to thickening of arteriolar walls. Unknown cause and poor

prognosiso Clinical- same as aboveo Dx- Cardiac Cath, PFTs showing restrictive pattern, EKG shows RVHo Tx- IV prostacyclins and CCB. A/C with warfarin due to venous stasis

Lung Transplant if qualified Cor Pulmonale-

o Usually due to COPD but other causes are anything that has lung pathologyo Clinical: clubbing, cyanosis, DOE, RV failure, Sternal lift, Polycythemiao 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 obstructionwheezeo Dx- Mimic bacterial pneumonias, Atelectasis possible tooo 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, echoo 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, Broncho 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 necessaryo Bronch can help identify bleeding source. o Tx can be bronch artery embolizationo 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

contraindicatedo 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 SCREENINGo 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 Crohn’s BOTH but UC higher risk. 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.

Gardner’s- 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- Duke’s Criteria- CT of abdomen and CXR. Stage A= muscularis mucosa.

Stage B= no nodal involvement but through MM. Stage C= nodes Stage D=metso Tx- Resect bowel WITH lymphatics AFTER OBTAINING BASELINE CEA

Duke’s 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 presentationo 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 CADo 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 foldso Tx- IVF and ABX. Papaverine infusion into SMA is tx of choice. OR direct intra-

arterial 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

Ogilvie’s Syndrome- NO mechanical obstruction, but radiography shows signs of obstruction.

o Causes- Recent surgery, trauma, serious illness (cancer/sepsis)o OBSTRUCTION MUST BE EXCLUDEDo 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 TMCo Tx- d/c abx, metronidazole + oral vanc. Cholestyramine can improve diarrheao Complications: Toxic Megacolon, Perforation, Electrolyte disturbances

Colonic Volvulus-

o Twisted bowel around its mesenteric origin resulting in possible obstruction or vascular obstruction (necrosisperforation)

o 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, anorexiao 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 Child’s 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)

Wilson’s 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 elevationo 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 tumoro 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 COMMONo 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 CONTRAINDICATEDo 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 unresectableo FibroLamellar- NOT assoc with Hep B or C, resectable (longer survival), young

adults commonly

o Risk Factors: cirrhosis, aflatoxin/vinyl chloride, A1AT, Hemo/Wilson’s, Schisto, Hepati Adenoma, Cigs

o 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.

Gilbert’s- 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 paino Dx- Arteriogram. Upper GI endoscopy shows blood out Ampulla of Vater. o Tx- volume replacement. Surgery to ligate arteries if necessary

Liver cysts- o Polycystic Liver Cysts- AD and assoc with ADPKD (usually cause of death).

Usually asymptomatic but sometimes pain or mass in RUQ. Tx unnecessaryo 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 Venographyo 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 specifico Mild elevation- acute alcoholic hepatitis or chronic viral hepatitiso Moderate- (high hundreds to thousands)- acute viral

o Severely- >10k- hepatic necrosis due to severe viral, shock liver or acetaminophen

o Mnemonic for ALT/AST elevation in asymptomatic: o 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 don’t know about stones:

o Cholesterol stones also associated with Native American Ancestry and CFo Pigment Stones assoc with hemolysis or alcoholic cirrhosiso Mixed stones exist (majority of stones)o 1/3 pts with biliary colic develop acute cholecystitis within 2 yrso 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 cholecystitiso Perforated Gallbladdero Emphysematous Cholecystitiso Cholecystenteric Fistulagallstone ileuso 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, AMSo 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 cholangitis-

Gallbladder 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.

o Presenting Symptoms: jaundice and pruritisobstructive jaundiceo 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 failureo Autoimmune and associated with other autoimmune diseases- middle age

womeno 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 pruritiso 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/cholangitiso U/S is best non-invasive test. ERCP for definitiveo 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 Pancreatitis-o Inflammation from prematurely activated enzymes invoking autodigestion. o Causes- GET SMASHED- Gallstones, ethanol, trauma, scorpion sting, mumps,

steroids, autoimmune, hypertrigs, ERCP, Drugso Clinical- epigastric abd pain, radiating to back of steady, severe, dull onset.

Worse after meals.. Fever, tachy, distention, ABSENT BOWEL sounds. Cullen’s (periumbilical), Gray Turners (flank), Fox (inguinal ligament).

o Dx- amylase/lipase, LFTs (for gallstone cause), Ranson’s 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 ductso 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, Courvoisier’s 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 Barret’s. 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 Diseaseo 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- bird’s 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 Hernia-

o 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. Tx- esophageal dilation and iron supplements

Schatzki’s 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 fundopo 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 Boerhaave’s.

o Pain, tachy, hypoTN, Hamman’s Sign (mediastinal crunch on breathing), Pneumothorax, Effusion.

o Dx- Soluble Gastrograffin swallowo 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 symptomso 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 (anti-parietal 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 layerso Polypoid Carcinoma- solid mass projects into stomach lumeno Superficial Spreading- best prognosiso Linitis plastica- leather bottle, through all layers early, thick rigid wall. WORST

ONEo Dx- Endoscopy with bxStaging with Abdominal CT. o Tx- Resect w/ >5cm marginso Blumer’s Shelf- mets to the rectum palpable on rectal exam

o Irish’s Node- mets to the left axillary nodes. Hyperthyroid-

o 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 Plummer’s Disease- toxic multinodular goiter- hyperfunctioning areas (decreased TSH levels). Rest of thyroid doesn’t function. Pathcy appearance on uptake scan. Common in ELDERLY pts

o Subacute Thyroiditis- exquisitely tender gland after a viral illnesso Hashimoto’s Thyroiditis- can cause TRANSIENT hyperthyroido 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 DOESN’T 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 hyperthyroid- o PTU/Methimazole inhibit T4 synthesis. PTU also inhibits peripheral conversion

to T3. Major S/E is agranulocytosiso B-Blockers- symptomatic managemento Radioactive Iodine Ablation- most common tx for Graves in US. Complication is

hypothyroidism. Administer a second dose in 6-12 mos if first doesn’t work. CONTRAINDICATED DURING PREGGO/BREASTFEEDING

o Surgical- subtotal—effective but possible permanent hypothyroid/hypoPTH, recurrent laryngeal nerve injury, recurrence of hyperthyroid

Must monitor calciumo 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

Symptomso Tx- IVF, cooling blankets, GLUCOSE + antithyroid (PTU q2h) and iodine (to inhibit

TH release) Hypothyroid-

o Insidious onset and many times asymptomatico Causes include Hashimoto’s, Iatrogenic and secondary hypothyroid.o You know the signs/symptoms already

o Dx- High TSH in primary, low TSH in secondary hypothyroidism. Hashimoto’s 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 Thyroiditis-o Follows viral illness- transient hyperthyroid (leakage of enzymes) followed by

euthyroid state and then hypothyroid (due to depletion of enzymes)o PAINFUL, TENDER THYROIDo Dx- Radioiodine uptake LOW (damaged cells can’t 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 Grave’s by low radioactive iodine uptake. Similar to

subacute thyroiditis except without the pain Chronic Lymphocytic Thyroiditis (Hashimoto’s)- 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-Thyroglobulino 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 diametero 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 Cancer-o Head and neck radiation during childhood. o Gardner’s Syndrome for papillary cancero MEN Type II- medullary cancero 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 levelso Tx- Transsphenoidal resection unless prolactin (medical management)

HyperProlactinemia- inhibits GnRHdecreased estrogen/testosteroneo Causes include prolactinoma, pregnancy, hypothyroid, psych medications,

verapamilo Men get decreased libido and gonad size with galactorrhea and visual signso Women- menstrual problems, dyspareunia, vaginal dryness. o Dx- high prolactin, MRI brain, TSH, pregnancy testo 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 hyperhidrosiso 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 Rathke’s Pouch. 20-25% of pit lesionso Bitemp hemianop. Brain MRI is diagnostic. Tx- surgery. Can cause

hyperprolactin, DI, or panhypopituitarism Diabetes Insipidus-

o Central- idiopathic, trauma or destructive process (Tb, sarcoid, tumor, syphilis)o Nephrogenic- hypoK, hypercal, lithium, demeclocycline, pyeloo HYPERNATREMIA MILD but polydipsia and polyuria commono 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-

o 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/deatho CHRONIC hyponatremiaasymptomatic or nausea/vomiting. Less commonly

CNS symptoms. o Dx- water load testo 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 Insufficiency-

o Primary (Addison’s)- 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 diseaseo 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.

o Dx- High levels of 17-OH Progesterone in serumo 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 140-200o 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, retinopathyo 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.

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 lossulcerscharcot’s joints, allodynia (hypersensitivity to light touch)

Mononeuropathies- secondary to nerve infarction. Autonomic Neuropathy- impotence, neurogenic bladder,

gastroparesis, constipation Dawn Phenomenon and Somogyi Effect-

o Morning hyperglycemiao 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: Stroke-

o 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 monthso Risk Factors- age and HTN. Other less impt ones smoking, DM, HLD, Afib, CAD,

FHx, carotid bruito 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.o 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 Stroke- o 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, ABC’s, 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.

Parkinson’s Disease-o 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, reserpineo 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 doesn’t respond to meds

o Difference btwn Progressive Supranuclear palsy and Parkinsons: PSP does not cause tremor, but causes ophthalmoplegia.

Huntington’s Chorea-o Chorea, personality changes, impaired mentation (progressive dementia),

Unsteady gait, Incontinenceo MRI shows atrophy of caudate. Tx is symptomatic though dopamine blockers

may help chorea and psychosis. Tremor-

o 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,

o Friedrich’s 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. Friedrich’s + telangiectasias. Increased cancer incidence.

o Tx- underlying cause Tourette’s Syndrome- OCD assoc. Onset b4 21 yrs old. AD inheritence.

o Motor or phonic tics.o Tx- clonidine, pimozide, haldol

Dementia- Things you don’t already knowo Binswanger’s Dz- insidious onset due to diffuse subcortical white matter

degeneration seen in pts with long-standing HTN and atherosclerosis. o Pick’s Dz- clinically identical to Alzheimer’so Pseudodementia- severe depression causes decline in cognition difficult to

distinguish from Alzheimer’s. Responsive to antidepressants. Alzheimer’s Dz-

o Risks include family hx or Down’s 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. Can’t 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 it’s worse due to 4x/daily dosing.

Dementia with Lewy Bodies- Alzheimer’s + Parkinson’s with more rapid progression than Alzheimer’s. Visual hallucinations predominate with some extrapyramidal features and fluctuant mental status. Sensitive to adverse effects of neuroleptics. Tx is with alzheimer’s drugs but also with neuroleptics.

Deliriumo Medical disturbance or condition resulting in RAPID cognitive dysfxn,

disorientation, perception abnormalities (hallucinations), slow-blunted responseo PDIMMWIT- Postop state, dehydration, infection, meds, metals, withdrawal,

infammation, traumao Dx- MMSE, Labs (chem, B12, thiamine), LP unless contraindicationso 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. o Bilateral fixed, dilared pupils= SEVERE ANOXIAo Unilateral Fixed Dilated Pupil- CN III compression with herniationo 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 SAHo 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 + Babinski’so Dx- CT Scano 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. 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, tachyo Signs of recovery in 1-3 wks is good prognosis. If >6 wks, then relapsing

syndrome is likely. o Dx- CSF shows elevated protein (Ig’s) 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 tumorso Infiltrate brain and have indistinct boundarieso Spread along White matter tracts- can cross corpus callosumo 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 well-

defined 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:o Hypercapniavasodilation (exacerbating problem of already increased IV

volume in the cranium) Key features of Traumatic Brain Injury-

o 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/rhinorrheao Coup Injury- injury at site of impacto 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 FVC’s and have a LOW THRESHOLD FOR INTUBATION (1L FVC)

Duchenne’s- X-linked recessive mutation of dystrophin. No infglammation. o Progressive, symmetric weakness that starts in childhood. Proximal muscles.o Eventually involves the respiratory muscles. GOWER’s +o Calf pseudohypertrophy. Wheelchair boundresp failuredeath in 3rd decadeo 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 café 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 commono 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 associatedo 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 Meniere’s 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 M’s, 4 I’s)- Metabolic, Masses, Missing Drugs (antiepileptic noncompliance or

withdrawal from alcohol etc), Miscellaneous (pseudoseizures- psychiatric in origin with normal EEG, Eclampsia, HTNsive encephalopathy).

Intoxications, Infections, Ischemia, Increaed ICPo 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 nodso 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 doesn’t 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, lumbosacralo Tx- supportive. Riluzole- glutamate blocking agent delays death by 3-5 mos

DDx for Bell’s Palsy- Trauma, Lyme, Tumor (acoustic neuroma), Guillain Barre (b/l), Herpes Zoster

o Dx- Clinicalb but consider Lyme in endemic areaso 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/vasculitiso 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- Sjogren’s, 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/Co 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.

o Diffuse- widespread skin involvement, rapid onset after Raynaud’s starts, visceral involvement including lungs, heart, GI and kidneys. ANA but lacks anti-Centromere. 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 Raynaud’s starts. ANTI CENTROMERE

o Clinical: Raynaud’s 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 Raynaud’s- can also use calcium channel

blockers. o Sjogren’s- autoimmune disease seen in women in which lymphocytes destroy salivary

and lacrimal glands, but can also involve, skin, lungs, thyroid, livero Primary- dry eyes and mouth with lymphocytic infiltration of minor salivary

glands (on histology). NO other rheumatologic diseaseo Secondary- dry eyes/mouth and ANOTHER connective tissue disease. o Clinical:

Dry eyes/mouth, arthritis/algias, Interstitial nephritis or vasculitiso Dx- ANA + , Ro, La +, o Tx- pilocarpine (enhances secretions), artificial tears, oral hygiene,

NSAIDs, steroids for arthritiso Rheumatoid Arthritis-

o Variants- Felty’s- anemia, neutropenia, splenomegaly and RA Still’s 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 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 Sjogren’s Xerostomia Rheumatoid Nodules (extensor surfaces) can also be in lungs, pleura or

pericardium)o Dx- RF titers correlated with severeity of disease. Anemia of chronic disease

present. o Tx- prevent/halt destruction. Do exercise along with pharmacological tx

Symptomatic- NSAIDs for pain Steroids if NSAIDs don’t work, but make them short term and

low dose. DMARD’s- page 248