Andrew Reid PA-C
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TABLE OF CONTENTS INTRODUCTION .................................................................................... 1 CHAPTER 1: CARDIOLOGY ................................................................. 2
-REVIEW QUESTIONS ................................................................................................. 34 -REVIEW ANSWERS .................................................................................................... 37 -QUICK FACTS/ASSOCIATIONS ................................................................................. 43
CHAPTER 2: PULMONOLOGY ............................................................. 46 -REVIEW QUESTIONS ................................................................................................. 71 -REVIEW ANSWERS .................................................................................................... 74 -QUICK FACTS/ASSOCIATIONS ................................................................................. 79
CHAPTER 3: MUSKULOSKELETAL/RHEUMATOLOGY .................... 81
-REVIEW QUESTIONS ................................................................................................. 120 -REVIEW ANSWERS .................................................................................................... 124 -QUICK FACTS/ASSOCIATIONS ................................................................................. 131
CHAPTER 4: GASTROENTEROLOGY ................................................. 135 -REVIEW QUESTIONS .................................................................................................. 166 -REVIEW ANSWERS .................................................................................................... 169 -QUICK FACTS/ASSOCIATIONS ................................................................................. 174
CHAPTER 5: REPRODUCTION ............................................................. 176 -REVIEW QUESTIONS .................................................................................................. 210 -REVIEW ANSWERS ..................................................................................................... 213 -QUICK FACTS/ASSOCIATIONS ................................................................................. 218
CHAPTER 6: GENITOURINARY ............................................................ 220 -REVIEW QUESTIONS .................................................................................................. 252 -REVIEW ANSWERS ..................................................................................................... 255 -QUICK FACTS/ASSOCIATIONS ................................................................................. 260
CHAPTER 7: EENT ................................................................................ 262 -REVIEW QUESTIONS .................................................................................................. 293 -REVIEW ANSWERS .................................................................................................... 295 -QUICK FACTS/ASSOCIATIONS ................................................................................. 299
CHAPTER 8: ENDOCRINOLOGY .......................................................... 301 -REVIEW QUESTIONS .................................................................................................. 319 -REVIEW ANSWERS ..................................................................................................... 322 -QUICK FACTS/ASSOCIATIONS .................................................................................. 327
CHAPTER 9: NEUROLOGY ................................................................... 329 -REVIEW QUESTIONS .................................................................................................. 350 -REVIEW ANSWERS ..................................................................................................... 353 -QUICK FACTS/ASSOCIATIONS .................................................................................. 358
CHAPTER 10: HEMATOLOGY .............................................................. 360 -REVIEW QUESTIONS .................................................................................................. 378 -REVIEW ANSWERS ..................................................................................................... 381 -QUICK FACTS/ASSOCIATIONS ................................................................................. 385
TABLE OF CONTENTS CHAPTER 11: PSYCHIATRY ................................................................. 387 -REVIEW QUESTIONS .................................................................................................. 403 -REVIEW ANSWERS ..................................................................................................... 405 -QUICK FACTS/ASSOCIATIONS ................................................................................. 408
CHAPTER 12: DERMATOLOGY ............................................................ 409 -REVIEW QUESTIONS ................................................................................................... 434 -REVIEW ANSWERS ...................................................................................................... 436 -QUICK FACTS/ASSOCIATIONS ................................................................................... 440
CHAPTER 13: INFECTIOUS DISEASE .................................................. 442 -REVIEW QUESTIONS ................................................................................................... 463 -REVIEW ANSWERS ...................................................................................................... 466 -QUICK FACTS/ASSOCIATIONS ................................................................................... 477
INTRODUCTION Medicine can be overwhelming, but it’s not complicated. What makes it so challenging is the amount of information you are expected to retain. So, what do you need to know and what can you ignore? This book will give you a straight forward way to learn the many disease processes out there. I didn’t write a lot of bullet points with a lot of random facts. Instead, I wrote down what is done first, and what will be done next. The boards want to make sure that you know the order in which to do things, even though everything is usually done simultaneously in clinical practice. This book contains everything you need to know to pass your boards. The first section of each chapter is filled with all the diseases required by the NCCPA blueprint. The second section is a set of review questions that goes over the entire chapter. The third section is a set of tables that detail important facts and associations. This third section is a nice way to rapidly review everything the night or morning before an exam. Purchasing this book is much more than just a book purchase. You will also have access to me should any questions arise. If there are ever any questions or clarification that is needed, please don’t hesitate to email me:
[email protected] I am here to make this process as painless as possible. I am here to help you. I took a great deal of time to put this together, and I know it will help. Study hard. Visualize your self passing. Go in with confidence. Before you know it, you will be out in clinical practice helping others. Always believe in your abilities, and remember: “Every artist was first an amateur” - Ralph Waldo Emerson
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Andrew Reid PA-C
1 Cardiology
“Whenever a doctor cannot do good, he must be kept from doing harm” – Hippocrates
Retrieved from https://flic.kr/p/FM2Hj
Congestive Heart Failure (CHF)
Introduction
Heart failure is a pump problem. There may be a problem with filling (diastolic dysfunction) or a problem with pumping (systolic dysfunction). The net result is a decrease in perfusion to tissues, resulting in under-oxygenation. Diastolic dysfunction: Decreased filling due to poor relaxation of the ventricle. Because the problem here is filling, and not pumping blood out, the ejection fraction will remain normal. Systolic dysfunction: Decreased ejection fraction usually less than 50%. This percentage correlates to the amount of blood that leaves the left ventricle (50% of the blood is pumped out of the ventricle). The most common etiology is coronary artery disease.
Signs and Symptoms
The most common presenting symptoms of heart failure are fatigue and shortness of breath. This is largely a clinical diagnosis based on a good history and physical exam. Other key features that lead you to the diagnosis are: orthopnea (SOB upon lying), paroxysmal nocturnal dyspnea (sudden feeling of suffocation mid sleep prompting the patient to get out of bed), pedal edema, jugular venous dystension, and an S3 gallop.
Diagnostic Testing The first and most useful test that should be performed is an echocardiogram. An ECG should be done to screen for arrhythmias and to look for Q waves (old in-farct). ECG might also show signs of ischemia and/or left ventricular hypertrophy. Stress testing is used to asses exercise tolerance and risk stratification. Chest X-ray is used in the evaluation of dyspnea (not to diagnose CHF).
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Treatment
ACE/ARBs and beta blockers are your main drugs in terms of lowering mortality. Specific beta blockers you should know are carvedilol, bisoprolol, and metoprolol succinate - these have the most proven benefit in reducing mortality. Small caveat: never give beta blockers during an acute exacerbation. Diuretics are given to reduce symptoms: fluid overload. Digoxin is also used for symptom control such as SOB. Digoxin decreases the time spent hospitalized, but does not reduce mortality in patients. Spironolactone or eplerenone (less endocrine side effects than spironolactone) are only beneficial to those who are classified as having class 3 or class 4 CHF. Be careful with the use of calcium channel blockers, as they may increase mortality in CHF patients. For those patients who continue to be symptomatic, the addition of nitrates and hydralazine has proven benefit (more so with African Americans). An ICD (implantable cardiac defibrillator) is used when the ejection fraction is below 35%, those with sutained VT, and/or those with unexplained syncope to prevent a fatal arrhythmia. Caveat: An ICD should only be used if the patient is expected to survive for at least one year. If everything up to this point has failed, the final option includes transplantation.
ACUTE EXACERBATION An ECG is done to look for arrhythmias and myocardial infarction. What about BNP? Well, this is used as an attempt to distinguish between CHF exacerbation and COPD exacerbation as the cause of dyspnea. This is a sensitive, but nonspecific test. Meaning, a normal BNP will exclude CHF, but an elevated BNP can be caused by a variety of reasons. A severely elevated BNP (>400) increases the likelihood of CHF exacerbation; 60 years of age are treated when the systolic pressure is over 150 or the diastolic is over 90 (unless they have diabetes or CKD - they are then treated when pressures rise >140/90). Hypertension also requires that it be elevated on at least two separate occassions. There are two stages of hypertension: Stage 1
Systolic: 140-159
Diastolic: 90-100 Stage 2
Systolic: over 160
Diastolic: over 100
Etiology
Over 95% of hypertension is termed essential (meaning idiopathic or no one really knows why). The other 5% are from secondary causes. The most common secondary cause is from renal disease. If a person states they regularly have a normal BP at home, but elevated in the office, they might suffer from white coat hypertension. The numbers at home are valid.
Signs and Symptoms
Patient are usually asymptomatic at the time of diagnosis. Hypertension does not cause headache!
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Diagnostic Testing
After diagnosis, it is important to look for end organ damage. Routine labs that are ordered include: urine analysis, urine micro albumin, EKG, CBC, BMP, and lipid panel. The physical should focus on: fundoscopy (hemorrhage or papilledema), thyroid assessment, carotid bruit, size and rhythm of heart, crackles in lungs, renal bruit, pedal edema, confusion or weakness.
Treatment First, initiate lifestyle recommendations such as weight loss, DASH diet,smoking cessation, moderate alcohol use, decrease sodium consumption, and exercise. If these do not work, a young healthy adult should be treated with a diuretic (hydrochlorothiazide or chlorthalidone), ACE/ARB, or a long acting dihydropyridine (amlodopine). Those in stage two should be treated with 2 medications (usually one will include a diuretic). If a person has co-morbid conditions, then the first line therapy is dictated by that condition: Diabetes: ACE/ARB
CHF/Ischemia/CAD: Beta blocker or ACE/ARB
Angina: Beta blocker or calcium channel blocker
BPH: Alpha blocker
Hyperthyroid: Beta blocker
CKD: ACE/ARB
Reynauds: Calcium channel blocker
Migraine: Beta blocker or calcium channel blocker Resistant hypertension is hypertension that is not responsive to at least three medications, one of which must include a diuretic.
Secondary hypertension
So, who should undergo evaluation for secondary hypertension?
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•Severe or resistant hypertension
•Age less than 30 who are otherwise healthy
•Malignant or very rapidly occurring hypertension
Renovascular hypertension is the most common cause of secondary hypertension. Clues to diagnosis: Renal artery stenosis: abdominal bruit
Hyperaldosteronism: hypokalemia and hypernatremia Primary kidney disease: elevated creatinine
Pheocromocytoma: acute episodes of elevated BP with headache, palpitations, and sweat-ing Cushings: moon face, central obesity, buffalo hump, proximal muscle weakness Sleep apnea: Obese men who snore
Coarctation of aorta: hypertension in a child. Hypertension of upper extremeties, diminished femoral pulses, and decreased blood pressure in the lower extremeties.
HYPERTENSIVE URGENCY
Introduction Severely elevated hypertension is considered to occur when the systolic is over 180 and/or when the diastolic is over 120.
Signs and Symptoms
By definition, the patient is asymptomatic and cannot have end organ damage.
Treatment
Do not bring down blood pressure rapidly, and do not use sublingual nifedipine (this is con-
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traindicated)! When a patient’s body is used to having elevated pressures, and then suddenly those pressures drop, there won’t be enough pressure to circulate oxygen to the brain and heart. This decrease in oxygenation can lead to MI or CVA, and has been most described with sublingual nifedipine. A gradual reduction over 1-2 days is the preferred approach. The general consensus is to initiate control with two BP medications and follow up in 2 days as an outpatient. There isn’t an agreement for the ideal first line medication.
HYPERTENSIVE EMERGENCY
Introduction Severely elevated hypertension usually over 180/120.
Signs and Symptoms
A hypertensive emergency must include end organ damage. Two subcategories under the hypertensive emergency include: malignant hypertension and hypertensive encephalopathy. Malignant hypertension will present with papiledema, exudates, retinal hemorrhage, acute kidney injury (hematuria or proteinuria), and/or focal neurological findings. Encepalopathy will present with cerebral edema: Headache, N/V, confusion, seizure, coma.
Diagnostic Testing
When there are focal neurological findings, an MRI should be done to rule out stroke.
Treatment The goal is to decrease the diastolic pressure to 100 in 6 hours. After the blood pressure has been controlled, begin oral therapy to bring the diastolic .20)
No Treatment
No treatment if patient is asymptomatic. PR progressively lengthens, until it fails to produce a p wave Pacemaker if symptomatic (signs of and QRS complex. hypo perfusion) Patient will have a continuously Treat everyone with a pacemaker to dropped QRS complex just like prevent progression to complete block. Mobitz 1, however, no lengthening of the PR is noted. May present with syncope Signal from the atria does not reach the ventricle. Therefore, you will have P waves that are Treat with a pacemaker. May be fatal. independent from the QRS complex
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BUNDLE BRANCH BLOCK
Right bundle branch: electrical activity in the his-purkinje fibers are slowed. The right bundle receives most of the blood supply from LAD. Wide QRS (over .12), RSR pattern in leads V1 or V2, S wave wider than R wave in V5 and V6. There may also be altered ST segments and T waves. Asymptomatic patients do not need treatment. Those who develop symptoms due to other electrical conductions should be placed on a pacemaker. Left bundle branch: Same pathophysiology as the right bundle branch, however, the left is instead affected. Wide QRS (over .12), notched R wave in V5 and V6. ST and T waves displacement are opposite to the direction of the QRS complex. Remember, a new LBBB must be treated as an MI when infarction is being considered. Treatment is the same as a right bundle branch block.
PAROXYSMAL SUPRAVENTRICULAR TACHYCARDIA
These are supraventricular tachycardias that are intermittent and occur abruptly. Patients will present with abrupt onset of palpitations and the EKG will show a narrow complex tachycardia. The first step is to assess hemodynamic instability (hypotension, SOB, chest pain, and altered mental status). If hemodynamic instability exists, then cardiovert. If stable, the patient may be given vagal maneuvers to slow down the rate (valsalva or carotid massage). This will allow you to see the P waves, as they are usually superimposed into the QRS complex. If this does not work, adenosine may be given, and will be diagnostic and therapeutic. Note: If the diagnosis is thought to be WPW, the addition of adenosine will worsen the arrhythmia and may lead to ventricular tachycardia and ventricular fibrillation.
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PREMATURE BEATS PVC Ectopic beats originating in ventricular foci. Patients are usually asymptomatic, but if symptoms occur, they will present with palpitations. The EKG will show a wide complex QRS without P waves. Following the wide complex QRS, there will usually be a compensatory pause (the AV node will be blocked for a short period not allowing the signal from the SA node to reach the ventricle). The AV node then clears, and a normal p wave and QRS complex are seen. Asymptomatic patients do not require treatment. Those who are symptomatic may be given a beta blocker.
PAC Ectopic beats originating from the atria outside the SA node. Patients are usually
asymptomatic, but if symptoms occur, they will present with palpitations. The EKG will
show a P wave before expected and will have a different morphology from the previous P waves. The closer the ectopic foci is to the SA node, the more similar the P wave will appear. Asymptomatic patients do not require therapy. If symptoms occur, treat with a beta blocker.
SICK SINUS SYNDROME
This is SA node dysfunction, usually from fibrous tissue covering the SA node. EKG will show: alternating bradycardia and tachycardia, sinus arrest without an appropriate escape rhythm, and an inappropriate response to stress. Symptoms are very inconsistent, and not helpful in the diagnosis. Treatment is with a pacemaker.
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VENTRICULAR TACHYCARDIA
WIDE COMPLEX TACHYCARDIA (requires at least 3 consecutive wide complexes). Do not try and differentiate between SVT or aberrant conduction. Always treat a wide complex tachycardia as ventricular tachycardia. If unstable, cadiovert. If stable treat with amidorone or procainamide. If medication does not convert to sinus rhythm, then cardiovert. Torsades de pointes:
This is a polymorphic ventricular tachycardia that arises from a prolonged QT interval. In the technical sense, if the baseline QT interval was normal, it is simply referred to as polymorphic ventricular tachycardia. Treatment: withdraw the offending drugs, correct electrolyte abnormalities, and cardiac pacing. Magnesium sulfate may be offered in the acute setting for drug induced torsades.
VENTRICULAR FIBRILLATION
No organized electrical activity.
Cardioversion immediately -> cpr->shock->epinephrine->shock->amiodarone
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STABLE ANGINA AND PRINZMETAL ANGINA
Introduction
Stable angina is myocardial ischemia secondary to exertion (increased oxygen demand). A variant, known as prinzmetal angina, is ischemia secondary to coronary artery spasm.
RISK FACTORS: hypertension, smoking, hyperlipidemia, diabetes, and obesity.
Signs and Symptoms Stable angina presents as chest discomfort with exertion and is relieved by rest or nitroglycerin. The discomfort is predictable in nature, and never occurs at rest. The physical exam will usually be normal. This is a diagnosis based on the patient’s history and risk factors for coronary artery disease. Prinzmetal angina typically occurs at rest.
Diagnostic Testing The ECG will be normal in stable angina. The ECG in prinzmetal angina will show ST segment elevations that will return to baseline immediately after the episode (usually 5-15 min). Neither will have elevated cardiac enzymes (STEMI will have elevated enzymes, and will not have the ST segment return to baseline so quickly). If the diagnosis is unclear, refer the patient for stress testing. Stress testing (either with medication or treadmill) will increase oxygen demand, and will demonstrate ischemia on ECG.
Treatment
Treat with lifestyle modifications (same as those in the hypertension section). Also, make sure to control hypertension, diabetes, and hyperlipidemia. All patients are treated with an aspirin and beta blocker. The beta blocker will be used to slow the heart, allow increased ventricular filling, and reduce oxygen demand. The patient will also be given nitroglycerin (decreases pre load) to be used on an as needed basis for chest pain. Those who cannot be controlled with medication should be referred for angiography and revascularization. Only use calcium channel blockers when beta blockers are contraindicated, or as an adjunct to beta blockers.
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Prinzmetal angina will be treated with calcium channel blockers as the pathophysiology is spasm of the smooth muscle. Do not use beta blockers in prinzmetal angina as this can predispose the patient to a worsening in spasm from unopposed alpha receptors.
ACUTE CORONARY SYNDROME
Introduction This encompasses UNSTABLE ANGINA, NSTEMI, and STEMI. All will present identical and testing is necessary to arrive at the diagnosis. Remember, time is muscle, so the faster you treat, the better the outcome. Women and diabetics can present atypically without chest pain.
Diagnostic Testing ECG: Unstable angina and NSTEMI will have signs of ischemia (ST depression or T wave inversion). STEMI will have ST elevation of 1mm or more in at least two contiguous leads Remember to repeat the EKG every 10 minutes if ACS is suspected, as the initial EKG may be normal. The first EKG abnormality usually seen with infarction will be hyperacute T waves. Remember, that a new left bundle branch block should be treated as an infarction. Cardiac enzymes: CK-MB will rise after 4 hours, and will stay elevated for a couple days. Troponins (Preferred cardiac marker and troponin-I is most specific) rises after 4 hours but will stay elevated for up to two weeks. Most patients with negative enzymes can be excluded by 6 hours, but for those high risk patients, you should continue serial labs for 12 hours. Reinfarction is diagnosed if troponin increases over 20%. CK-MB can also be
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used to evaluate reinfarction, as the numbers should return to baseline after a couple days. CK-MB is now second line to diagnose reinfarction. Unstable angina will NOT have an elevation in cardiac enzymes.
NSTEMI and STEMI WILL have an elevation in cardiac enzymes.
Initially, unstable angina and NSTEMI will present identical, as it takes time for cardiac enzymes to rise.
Treatment
All patients presenting with ACS should immediately be given morphine, oxygen, nitrates (avoid if the patient is on phosphodiesterase-5 inhibitors – as this will cause hypotension),
and aspirin (chewed). Caveat: If patient has inferior MI, and suspected involvement of the right ventricle, avoid nitrates as this can cause a severe drop in blood pressure. All patients should also receive a beta blocker (metoprolol or atenolol) and a statin (atorvastatin) immediately if no contraindication exists. STEMI: Everyone gets heparin. PCI is the preferred to thrombolytics. PCI must be done within 90 minutes of arrival. If PCI is unavailable, or if unable to get to a center in 90
minutes, give thrombolytics. Thrombolytics are only indicated if chest pain has been present under 12 hours and lacks contraindications (coagulation disorder, severe hypertension, internal bleeding, or history of hemorrhagic stroke).
NSTEMI and unstable angina are managed identical to STEMI with the following exceptions: NO thrombolytics are given. Give either ticagrelor or GP IIb/IIIa inhibitor instead. Post STEMI/NSTEMI: all patients should be continued on aspirin, beta blocker (metoprolol or atenolol), ACE, and statin. Clopidogrel is used for those with aspirin allergy. Cocaine associated MI should be treated the same as those with other forms of ACS with the following modifications: Avoid beta blockers and give benzodiazepines.
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AORTIC ANEURYSM/DISSECTION
Introduction
Abdominal aortic aneurysm is a dilation of the aorta, usually below the renal artery. One time screening with ultrasound should be offered to men over 65 who have a history of smoking. Dissection is a tear in the aortic wall and is associated with Marfan syndrome and Ehlers-Danlos syndrome.
Signs and Symptoms
The majority of patients with AAA are asymptomatic. When patients have symptoms, they might present with abdominal or back pain. The exam will show a pulsatile abdominal mass. Dissection will present in an older man with sudden severe tearing chest pain or interscapular back pain.
Diagnostic Testing
AAA is diagnosed on ultrasound. Dissection may have a blood pressure differential between both arms. Widened mediastinum will be present on chest Xray. CT, MRI, and TEE are more specific than CXR.
Treatment
AAA:
Under 3 cm: No further workup
3cm-3.9cm require repeat ultrasound in 2-3 years
4cm-5.4cm require repeat ultrasound in 6 months
Over 5.5 cm should be surgically repaired. Dissection:
Type A = Ascending aorta=surgery
Type B = Descending aorta= beta blocker. Surgery is indicated if complete rupture or end organ damage.
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Imaging should then be done every 6 months to yearly to look for degeneration.
ARTERIAL EMBOLISM/THROMBOSIS
The majority will originate in the heart secondary to MI or AFIB, and will travel to the lower extremities. These emboli will lodge in areas of excess plaque formation or where there are bifurcations; the femoral artery being the most prevalent. Acute ischemia may cause pain, weakness, or numbness; however, the majority are from chronic plaque formation, allowing enough collateral circulation, to render the patient asymptomatic. Treatment for an acute embolism includes anticoagulant therapy.
Giant Cell Arteritis This is a vasculitis of the extracranial branches of the carotid artery. The patient will present with headache, jaw claudication, and visual disturbances. Exam will show scalp tenderness. The majority will be women over 50 and have an elevated ESR. A normal ESR virtually excludes the disease. Diagnosis is made with temporal artery biopsy.
Treated with prednisone to avoid blindness from optic nerve ischemia. Do not wait on biopsy results to start the prednisone if GCA is suspected.
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SYSTOLIC MURMURS
Aortic Stenosis
Usually seen in the elderly due to calcification of the aorta. The other two etiologies include congenital bicuspid/unicuspid valve and rheumatic disease
dyspnea, fatigue, and syncope.
Pulmonic Stenosis
The main etiology is mitral valve Mitral Regurgitation prolapse and coronary disease.
Most commonly from dilation of right atrium and ventricle
Heard best at the left upper sternal border and may have ejection click.
Patients are usually Murmur: asymptomatic, but holosystolic may have dyspnea murmur. Heard and fatigue. best over apex and radiates to axilla.
This is usually asymptomatic, but may cause chest pain, palpitations, and anxiety. Usually present in women
Mitral Valve Prolapse
Tricuspid Regurgitation
The most common symptoms include dyspnea, angina, dizziness. Patients may also present with syncope.
Systolic crescendodecrescendo murmur. Heard best at the second right intercostal space radiating to the neck.
Symptoms are nonspecific, might be those of right sided heart failure if present.
Murmur: Has a mid-systolic click, with a possible late systolic murmur depending on the severity of regurgitation present.
Patients who present with any symptoms need surgical correction immediately due to the high risk of sudden death. Treatment is with balloon valvotomy. If severe, then surgery is indicated. Asymptomatic patients are not treated. Those with symptoms are given vasodilators. If severe, worsening, or no improvement in symptoms with medications, the next step Is surgery.
Beta Blockers
Murmur: Diuretics are used holosystolic for symptoms. For murmur. Heard those with heart best left mid sternal failure, therapy border. When should be aimed at that. For severe regurgitation is severe, the murmur disease, surgery is performed. will fade. 25
DIASTOLIC MURMURS
Aortic Regurgitation
Pulmonic Regurgitation
Mitral Stenosis
Dilation of aortic root or congenital bicuspid valve. Outside the US the most common cause is rheumatic disease
Asymptomatic. Will present with wide pulse pressure (water hammer pulse).
Treatment is with surgery for those who are symptomatic, or those with progressive enlargement if asymptomatic.
Decrescendo murmur. Identical to aortic regurgitation.
Pulmonic hypertension Shortness of breath. Pregnancy will exacerbate symptoms, or Rheumatic disease cause initial symptoms in those who were asymptomatic
Rheumatic disease. Will Tricuspid Stenosis occur with other valve abnormality
Blowing quality. Will become holosystolic as the regurgitation worsens. Heard best at the left sternal border.
Symptoms are similar to other valvular disorders.
Low pitch rumble. Best heard at the apex.
Heard best at 4th intercostal space at the lower left sternal border.
Treatment is with balloon valvotomy or surgery. Diuretics and beta blockers may be used for symptom control only. Ace inhibitors and diuretics may be used for symptom control. If no improvement balloon valvotomy or surgery is done.
PERIPHERAL ARTERIAL DISEASE
Peripheral arterial disease is synonymous to coronary artery disease. The presentation is that of angina in the legs (leg pain with exertion and relieved with rest). This can be diagnosed with the ankle-brachial index. This is the ratio of the blood pressure in the ankles to the arm. This is a positive test when the ratio is under .9 (normally the blood pressures should be equal). All patients receive aspirin. Blood pressure, lipids, and glucose should be normalized, similar to those with CAD. The first step in treatment is a supervised 12 week exercise regimen. Cilostazol is the only medication that has any proven medical benefit for the treatment of PAD. PhysicianAssistantBoards.com
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PHLEBITIS/THROMBOPHLEBITIS This is a thrombus in a superficial vein, most commonly the saphenous vein, causing inflammation of the surrounding tissue. This usually develops in those with varicose veins. The patient will present with pain, tenderness, and erythema. A palpable cord (thrombus) will be felt. This is a clinical diagnosis, but a duplex ultrasound is done to rule out DVT. Treat with elevation, warm compress, compression stockings, and NSAIDs. Those with concomitant DVT or at high risk for DVT, should be treated with anticoagulation (low molecular weight heparin or warfarin) for four weeks instead of supportive therapy.
Deep Vein Thrombosis Introduction
Clot formation arising from Virchows triad: hypercoagulability, stasis, and endothelial injury. Virchows triad risk factors include OCP use, pregnancy, cancer, recent hospitalization, and/or immobilization. A small percent will not have risk factors and are termed unprovoked DVT.
Signs and Symptoms
The patient will present with unilateral lower extremity pain, erythema, and swelling. Homan sign will be positive on exam: calf pain with dorsiflexion of the ankle. In reality, this test lacks sensitivity and specificity and should never be used (but for exams this points to DVT).
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Diagnostic Testing Begin with wells criteria; if the patient has a score under 2 (meaning low probability) order a D-DIMER. A normal D-dimer virtually excludes all DVTs. An elevated D-dimer or a well score over 2 requires duplex ultrasound.
Treatment
Heparin and warfarin are started together. You must overlap the two medications for 5 days, as it takes a few days for warfarin to take effect. Also, warfarin inhibits protein C and S initially, and therefore might increase risk for clot formation the first few days. Continue warfarin for 3-6 months (INR should be 2-3). Those who have unprovoked DVT should be kept on warfarin indefinitely as long as there aren’t any contraindications.
VARICOSE VEINS
Defined as veins that become dilated over 3mm. Faulty valves causing blood to pool is the most common cause leading to dilation of the vein. Patients will often feel leg pain and swelling. Duplex ultrasound is done to evaluate reflux. Compression hose stockings and leg elevation are first line treatment followed by sclerotherapy.
VALVULAR DISEASE
The boards want you to know the murmur associated with these valvular disorders. A defi-nite diagnosis for all is reached with echocardiogram. Most symptoms are similar to that of CHF: shortness of breath and chest discomfort. Certain maneuvers will affect murmur intensity - know them: Inspiration increases right ventricular filling, but decreases left ventricular filling.
Right sided murmurs Increase with Inspiration.
Left sided murmurs increase with expiration.
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Squatting/leg raise/handgrip increases vascular resistance (afterload) and increases ven-tricular filling (preload). Increasing preload and afterload increases the sound of all mur-murs, except that of mitral valve prolapse (this will decreases). Standing and valsalva decrease venous return (preload). Decrease in preload decreases the sound of all murmurs, except that of mitral valve prolapse (this will increase). Systolic Murmur
Aortic Stenosis
Usually seen in the elderly due to calcification of the aorta. The other two etiologies include congenital biscupid/ unicuspid valve and rheumatic disease
Dyspnea, fatigue, and syncope
Pulmonic Stenosis
Mitral Regurgitation
The most common symptoms include dyspnea, angina, dizziness. Patients may also present with syncope.
The main etiology is mitral valve prolapse and coronary disease
Systolic crescendodecrescendo murmur. Heard best at the second right intercostal space radiating to the neck.
Patients who present with any symptoms need surgical correction immediately due to the risk of sudden death.
Heard best at the left Treatment is with upper sternal border balloon valvotomy. If and may have severe, surgery ejection click indicated.
Asymptomatic patients aren’t treated. Those with Asymptomatic. May Holosystolic murmur symptoms are given vasodilators. If have dyspnea and heard best over apex fatigue and radiates to axilla severe, worsening, or no improvement with meds, the next step is surgery.
Mitral Valve Prolapse
Asymptomatic. But, may cause palpitations, chest pain, and anxiety. Usually present in women.
Mid systolic click with possible late systolic murmur depending on the severity
Treat with beta blockers
Tricuspid Regurgitation
Symptoms are non specific. Symptoms can be the same as right sided heart failure
Holosystolic murmur heard best left mid sternal border. When regurgitation is sever, murmur will fade.
Diuretics for symptoms. Those with heart failure treat accordingly. Surgery in severe disease. 29
Most commonly from dilation of right atrium and ventricle
Diastolic Murmurs
Dilation of aortic root or congenital bicuspid valve. Aortic Regurgitation Outside the US the most common cause is rheumatic disease
Tricuspid Stenosis
Rheumatic disease
Rheumatic disease. Will occur with other valve abnormality
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Treatment is with surgery for those who are symptomatic, or those with progressive enlargement if asymptomatic.
Decrescendo murmur. Identical to aortic regurgitation.
Pulmonic hypertension
Pulmonic Regurgiation
Mitral Stenosis
Blowing quality. Will become Asymptomatic. Will holosystolic as the present with wide regurgitation pulse pressure worsens. Heard (water hammer best at the left pulse). sternal border.
Shortness of breath. Pregnancy will exacerbate symptoms, or cause initial symptoms in those who were asymptomatic
Symptoms are similar to other valvular disorders
Low pitch rumble. Best heard at the apex.
Treatment is with balloon valvotomy or surgery. Diuretics and beta blockers may be used for symptom control only.
Heard best at 4th intercostal space at the lower left sternal border
Ace inhibitors and diuretics may be used for symptom control. If no improvement balloon valvotomy or surgery is done
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ENDOCARDITIS
Introduction Infection of the endocardial surface of the heart, which extends to the heart valves. Risk factors include prosthetic heart valves and injection drug users.
Etiology
Streptococci viridans is the most common bacteria in prosthetic and native valves. Staphylococcus aureus is the most common bacteria in those who are injection drug users (vegetation will appear on the right).
Sign and Symptoms The patient will present with a new or change in murmur plus fever. Look for Jane way lesions (painless plaques on palms and soles), Osler nodes (painful nodes on fingers and toes), and/or Roth spots (pale retinal lesions surrounded by hemorrhage).
Diagnostic Testing The first thing to do is to obtain blood cultures (three separated by one hour). Make sure to obtain the blood cultures before antibiotics are given. Next, order an echocardiogram. DUKE CRITERIA:
Two major, or one major and three minor, or 5 minor:
Major: Positive blood culture, vegetations on echocardiogram, new regurgitant murmur
Minor: Fever, vascular phenomenom (emboli to organs), immunologic phenomenon (roth, osler,jane), or positive cultures of uncommon pathogen.
Treatment
Treat empirically with [ceftriaxone or vancomycin] AND gentamicin until cultures return. Then, treat according to the culture. Prophylaxis against endocarditis is done with amoxicillin and is indicated for those with
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•History of endocarditis
•Prosthetic valves
•Unrepaired cyanotic congenital heart disease.
•Cardiac transplant patients AND are undergoing: •Dental procedures that affect gingival tissue
•Invasive respiratory procedures
•Invasive treatment of skin infections
PERICARDITIS
Introduction Inflammation of the pericardium (two layers that cover the heart). The most common etiologies are idiopathic and viral.
Sign and Symptoms
The patient will present with pleuritic chest pain (worsened with inhalation) and positional chest pain (worse supine and improved with sitting). A friction rub is a very specific physical exam finding (grating sound heard with the bell of the stethoscope).
Diagnostic Testing The EKG will show diffuse ST elevations with PR depressions. The chest xray will show an enlarged cardiac silhouette. Troponins will be elevated, but do not signify infarction. An echocardiogram can distinguish between an MI and pericarditis. Pericarditis will have pericardial effusion and will not have wall motion abnormalities.
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Treatment
Treatment is with NSAIDs.
CARDIAC TAMPONADE
Introduction
This is a result of excess pericardial fluid, which exerts pressure onto the heart, leading to filling and hemodynamic compromise.
Sign and Symptoms
Patient will present with Becks Triad: hypotension, muffled heart sounds, and distended neck veins. Pulses paradoxus may also be present. This occurs when there is a drop in blood pressure of at least 10mmHg with inhalation.
Diagnostic Testing The EKG will show electrical alternans (QRS complexes alternate in amplitude). The chest Xray will show an enlarged cardiac silhouette and clear lung fields. The echocardiogram will show pericardial effusion and chamber collapse. Definitive diagnosis and treatment is done with pericardiocentesis.
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REVIEW QUESTIONS 1. How will the ejection fraction differ in diastolic and systolic heart failure? 2. What is the most common etiology in CHF? 3. What is the first test that should be ordered in the evaluation of CHF? 4. Which drugs lower mortality in heart failure? 5. Which beta blockers lower mortality? 6. What is the medication of choice for hypertrophic cardiomyopathy? 7. What sound will you hear in a patient with an ASD? 8. What classic x-ray finding will you see in coarctation of the aorta? 9. What classic murmur will be heard in patients with PDA? 10.What are TET spells? 11.What is Eisenmenger syndrome? 12.What is the most common cause of secondary hypertension? 13.What are the first line medications for hypertension in patients who are otherwise healthy? 14.What is the difference between hypertension urgency and emergency? 15.What is the classic clinical presentation for a patient in cardiogenic shock? 16.How will atrial flutter and atrial fibrillation present on EKG?
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17.What will happen if a patient who presents with WPW is accidentally given adenosine? 18.What is the classic presentation for a patient presenting with angina? 19.What are the medications of choice for patients with stable angina? 20.What is the treatment of choice for prinzemtal angina? 21.What will differentiate unstable angina from NSTEMI? 22.Why should you proceed with caution in administering nitrates in patients with an inferior MI? 23.What medications should be given to all patients post MI? 24.What do the guidelines say about screening for AAA? 25.Why should steroids be given to a patient with suspected GCA before doing a biopsy? 26.What is the only medication with proven benefit in peripheral artery disease? 27.What is the most common vein affected in patients with superficial thrombophlebitis? 28.What are risk factors for DVT? 29.When should a D-Dimer be ordered for DVT? 30.How does respiration affect murmurs? 31.What are the most common symptoms in a patient with aortic stenosis? 32.Which valvular abnormality will present with a water hammer pulse?
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33.What are the most common etiologies in endocarditis? 34.How will patients with endocarditis present? 35.What is the first test to order in patients with suspected endocarditis? 36.What is the classic EKG finding present in patients with pericarditis? 37.What is Becks triad and when will it be found?
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Review Answers 1.How will the ejection fraction differ in diastolic and systolic heart failure?
Diastolic dysfunction will have a normal ejection fraction. The problem here is poor relaxation leading to impaired filling. Systolic dysfunction will have a decreased ejection fraction. The problem here is poor contraction. 2. What is the most common etiology in CHF?
Coronary artery disease. ALL patients get aspirin, beta blockers, and a statin. 3. What is the first test that should be ordered in the evaluation of CHF? Echocardiogram. Remember, this is a clinical diagnosis, but the echocardiogram is used to give added information, such as: estimatating ventricular size and ejection fraction. It is NOT used to diagnose CHF. 4. Which drugs lower mortality in heart failure?
ACE/ARBs and beta blockers lower mortality in all patients with CHF. Spiranolactone and eplerenone lower mortality in those who have class 3 or class 4 disease. Diuretics and digoxin reduce symptoms only - they do not reduce mortality! 5. Which beta blockers lower mortality?
The only beta blockers that have proven benefit in CHF are carvedilol, bisoprolol, and metoprolol succinate (think succinate like survival - both start with “s”). 6. What is the medication of choice for hypertrophic cardiomyopathy?
Beta blockers. Do not confuse this with HOCM (also treated with beta blockers). Hypertrophic cardiomyopathy is a type of diastolic dysfunction. Diuretics are CONTRAINDICATED in HOCM, but not hypertrophic cardiomyopathy. 7. What sound will you hear in a patient with an ASD?
Systolic ejection murmur with wide splitting of S2.
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8. What classic x-ray finding will you see in coarctation of the aorta?
You will either see “rib notching” or a “3 sign”. 9. What classic murmur will be heard in patients with PDA?
Machine like continuous murmur. 10.What are TET spells?
These are found in patients with tetralogoy of fallot and are episodes of hyper cyanosis.
Classically, the child will bend down bringing their knees to their chest.
This will decrease venous return, increase vascular resistance making the child more comfortable. 11.What is Eisenmenger syndrome?
This is seen in patients with a VSD, meaning a shunt connecting both ventricles. Normally, the pressure is greatest in the left ventricle, which will push oxygenated blood to the right ventricle. Over time, this excess blood pushed to the right ventricle is too much for the lungs to handle. This will lead to pulmonary congestion. Eventually, this leads to increased pressure in the pulmonary vasculature, and in turn to the right ventricle (more so than the left ventricle). This will lead to a reversal of blood flow, from the right ventricle to the left. Deoxygenated blood will then leave the heart into the systemic circulation - this is bad! 12.What is the most common cause of secondary hypertension?
Renovascular disease 13.What are the first line medications for hypertension in patients who are otherwise healthy?
Diuretics, ACE/ARBs, or Amlodipine (long acting dihydropyridine). 14.What is the difference between hypertension urgency and emergency?
They will both have a blood pressure >180/120. The difference is that hypertension emergency will also have end organ damage. PhysicianAssistantBoards.com
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15.What is the classic clinical presentation for a patient in cardiogenic shock?
Hypotensive, altered mental status, and cool/clammy skin. 16.How will atrial flutter and atrial fibrillation present on EKG? Atrial flutter will have a regular rhythm with a saw tooth pattern. Atrial fibrillation will have an irregularly irregular rhythm without p waves. 17.What will happen if a patient who presents with WPW is accidentally given adenosine?
This may place the patient into ventricular tachycardia or fibrillation. 18.What is the classic presentation for a patient presenting with angina?
The patient will have chest pain that is relieved with rest or nitroglycerin. The chest pain is predictable and reproducible. New chest pain or worsening chest pain can never be classified as stable angina - this is unstable angina. 19.What are the medications of choice for patients with stable angina? All patients should receive a beta blocker, aspirin, and nitroglycerin. The beta blocker will increase filling time and decrease oxygen demand. The nitroglycerin is used on an as needed bases for chest pain relief. 20.What is the treatment of choice for prinzemtal angina?
Give these patients calcium channel blockers. Their pain is due to smooth muscle spasm. Avoid beta blockers, as this will result in unopposed alpha stimulation and worsen the their symptoms. 21.What will differentiate unstable angina from NSTEMI?
Both will clinically present the same. Both will have similar EKG findings. The only difference will be that NSTEMI will have elevated cardiac enzymes, while unstable angina will not. Most MIs can reliably be excluded after 6 hours, but if clinical suspicion is high, continue to monitor for 12 hours. The most specific cardiac marker
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will be troponin I. Troponin I is also now used to diagnose reinfarction - look for the trend. 22.Why should you proceed with caution in administering nitrates in patients with an inferior MI? If the right ventricle is involved, nitrates will cause a sudden and severe drop in blood pressure, as this area is preload dependent. 23.What medications should be given to all patients post MI?
Everyone leaves with an aspirin, beta blocker (metoprolol or atenolol), ACE inhibitor, and a statin. Clopidogrel is given to patients with aspirin allergy. 24.What do the guidelines say about screening for AAA?
Screen males over the age of 65 who have ever smoked. Only a one time screening with ultrasound is indicated. 25.Why should steroids be given to a patient with suspected GCA before doing a biopsy? Optic nerve ischemia can develop leading to blindness. Saving the patients eye sight is more important then confirming the diagnosis. 26.What is the only medication with proven benefit in peripheral artery disease?
Cilostazol 27.What is the most common vein affected in patients with superficial thrombophlebitis?
Saphenous vein 28.What are risk factors for DVT?
Know Virchows triad: hypercoagulability, stasis, and endothelial injury. If risk factors are not present, this is termed unprovoked DVT.
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29.When should a D-Dimer be ordered for DVT?
D-dimer is only ordered when there is a low clinical suspicion. If DVT is highly suspected, this should never be ordered. DVT has a high sensitivity, but horrible specificity. This means many things can elevate the value, but it is almost always elevated in patients with DVT. Remember, only order if the clinical suspicion is low. 30.How does respiration affect murmurs?
Inspiration will increase right sided murmurs. Expiration will increase left sided murmurs. Inspiration will increase right ventricular filling, but decrease left ventricular filling. 31.What are the most common symptoms in a patient with aortic stenosis?
Dyspnea, angina, and dizziness. 32.Which valvular abnormality will present with a water hammer pulse? Aortic regurgitation 33.What are the most common etiologies in endocarditis? Streptococcus viridans and staphylococcus aureus. Staphylococcus aureus is associated with patients who are injection drug users. 34.How will patients with endocarditis present?
They will have a new murmur or a change in murmur with a fever. 35.What is the first test to order in patients with suspected endocarditis?
Blood cultures! The echocardiogram is done after blood cultures have been collected. Antibiotics are given after three blood cultures separated by one hour have been collected. 36.What is the classic EKG finding present in patients with pericarditis?
Diffuse ST elevations with PR depression. An MI will have ST elevations, but they will not be diffuse.
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37.What is Becks triad and when will it be found?
Becks triad is found in patients with cardiac tamponade. The classic triad consists of hypotension, muffled heart sounds, and distended neck veins.
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QUICK FACTS/ASSOCIATIONS CONDITION
FACT/ASSOCIATION
CHF
Orthopnea, paroxysmal nocturnal dyspnea, jugular venous distention, S3
HOCM
Sudden death in athlete
Atrial Septal Defect
Fixed wide splitting of S2
Coarctation of Aorta
X-Ray: Rib notching, 3 sign
PDA
Machine like murmur
Tetralogy of Fallot
Cyanosis with crying or feeding
VSD
Holosystolic murmur
Cardiogenic Shock
Hypotensive, cool, clammy skin
Atrial Fibrillation
Irregular irregular rhythm
Atrial Flutter
Saw tooth pattern
AV Block
Long PR interval
Mobitz 1
Progressivly lengthening PR interval
Mobitz 2
Dropped QRS without lengthening
Third Degree Block
Independent P wave and QRS complex
Paroxysmal Supraventricular Tachycardia
Narrow complex tachycardia
Stable Angina
Chest pain relieved with rest
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CONDITION Prinzmetal Angina
FACT/ASSOCIATION Diffuse ST segment elevations, coronary artery spasm
ACS
Morpine, oxygen, nitrates, aspirin
Cocaine Induced MI
NO betablockers, give benzodiazepines
Aortic Aneurysm
Tobacco
Aortic Dissection
Marfan Syndrome, Ehlers-Danlos syndrome, tearing chest pain, Wide mediastinum
GCA
Jaw claudicaton, visual disturbance, >50 years of age
PAD
Leg pain relieved with rest, cilastazol
Superficial Thrombophlebitis
Palpable Cord
DVT
Virchows triad, unilateral LE swelling, pain, and erythema. Homan sign
Murmurs
Right side murmurs increase with inspiration. Left side murmurs increase with expiration
Aortic Stenosis
Systolic, second right intercostal space, radiates to neck
Mitral regurgitation
Holosystolic murumur
MVP
Women, anxiety, mid-systolic click
Aortic Regurgitation
Wide pulse pressure. Water hammer pulse
Endocarditis
New murmur, fever, injection drug use, streptococcus viridans , Jane way lesions, Osler nodes, Roth spots
Pericarditis
Pleuritic chest pain. Worse upon laying, improves with sitting. ST segment elevation, PR depression
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Condition
Facts/Associations
Cardiac Tamponade
Becks triad (hypotension, muffled heard sounds, distended neck vein), pulses paradoxus, electrical alternans.
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