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Andrew Reid PA-C

Physician Assistant
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PANCE/PANRE REVIEW

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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 its 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 didnt 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 dont hesitate to email me:

AndrewReid@PhysicianAssistantBoards.com

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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1
Whenever a doctor cannot
Cardiology 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 dysfunc-
tion) or a problem with pumping (systolic dysfunction). The net result is a decrease in per-
fusion 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), paroxys-
mal nocturnal dyspnea (sudden feeling of suocation 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 eects than spiro-
nolactone) 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 car-
diac 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 exac-
erbation 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;
<100 virtually excludes the diagnosis. Cardiac enzymes should be drawn, to look for an MI
as the cause of exacerbation.
Next, begin treatment with the acronym LMNOP:
Loop diuretics
Morphine
Nitrates

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Oxygen
Position (head up)/positive pressure

CARDIOMYOPATHY
Introduction
This is a disease of the heart muscle associated with cardiac dysfunction. The strict defini-
tion requires that no etiology is found (but most will usually have a genetic component).
Because there usually is no etiology, cardiomyopathies can be present during any decade
of life, including childhood. There are three main types: Dilated cardiomyopathy, hypertro-
phic cardiomyopathy, and restrictive cardiomyopathy. All of these can lead to heart
failure.

Signs and Symptoms


Symptoms will usually be identical to those discussed in congestive heart failure.

Diagnostic Testing
The echocardiogram is the test of choice to distinguish between the three.

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Specifics
Cardiomyopathy Introduction Dysfunction Treatment

Ventricle is dilated,
leading to decreased
Dilated Systolic Same as CHF
contraction of the
ventricle

Normal or impaired
ventricular filling with Beta Blockers, followed
Hypertrophic ventricular hypertrophy Diastolic by Calcium Channel
and preserved systolic Blockers.
function.

Impaired ventricular
filling without
hypertrophy of the
ventricle. Also has Diastolic dysfunction,
No specific Treatment
Restrictive impaired contractility. which can lead to
available
This is the least systolic dysfunction
common cause of
cardiomyopathy in the
states.

Distinguish hypertrophic cardiomyopathy from hypertrophic obstructive cardiomyopathy.


In HOCM, the septum will cause an obstruction to normal blood flow out of the aorta.
Classically, HOCM is the diagnosis when a young healthy athlete dies suddenly. However,
the most common symptom is shortness of breath, not death. This is also treated with
beta blockers; but do not use diuretics, as they are contraindicated in HOCM.

ATRIAL SEPTAL DEFECT


This is a direct connection between both atria through a defect in the septum. These chil-
dren are usually asymptomatic, but over time can lead to heart failure or recurrent
respira-tory infections. You will hear a systolic ejection murmur with a fixed wide splitting
of S2.
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The best test for diagnosis is an echocardiogram. The ASD will usually close spontane-
ously, but surgery may be performed at age 4 or in those who are severely symptomatic.

COARCTATION OF THE AORTA


Narrowing of the aorta at the ductus arteriosus. May present with hypertension or
respira-tory distress. There will be a reduced blood pressure and a reduced pulse in the
lower extremities. Diagnosed by echocardiogram. Chest x-ray will show rib notching or a
3 sign at the site of coarctation. These are surgically corrected.

PATENT DUCTUS ARTERIOSIS


The ductus arteriosis is a connection between the main pulmonary artery and the aorta. It
usually closes the first two days of life. The ductus arteriosis is kept open by a low
oxygen environment and prostaglandins. Failure to close is termed PDA. You will hear a
machine like continuous murmur. Diagnosis is made with echocardiogram. Premature
infants are treated with indomethacin. All others are treated with percutaneous catheter
closure or surgical ligation.

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TETRALOGY OF FALLOT
Cyanotic heart disorder that is characterized by:
Right ventricular hypertrophy
VSD
Overriding aorta
Right ventricular outflow obstruction

Harsh systolic ejection murmur heard best at the left sternal border.
Tet spells: hyper cyanotic episodes that develop during crying or feeding. Bringing the
childs knees to the chest will decrease venous return and increase vascular resistance,
which will in turn make the child more comfortable.

Diagnosed with echocardiogram. Treated by surgical repair.

VSD
A direct connection between both ventricles through a defect in the septum.
Eisenmenger syndrome: First, there will be a left to right shunting of blood, which will
eventually lead to pulmonary hypertension. As the pressures increase in the pulmonary
vasculature, more so than the right ventricle, a shunt reversal occurs. This means that
deoxygenated blood will be shunted from the right ventricle to the left and out into the
systemic circulation.
A holosytolic murmur is heard that does not increase with respiration. Diagnosed with
echocardiogram. This will usually close without treatment, but surgical repair is done for
symptomatic children.

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HYPERTENSION
Introduction
The definition is a systolic pressure over 140 or a diastolic over 90. Diabetes and CKD are
treated to the same value. Patients >60 years of age are treated when the systolic pres-
sure 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 ele-
vated in the oce, they might suer 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 or-
dered 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, confu-
sion 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, bualo 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 patients body is used to having elevated pressures, and then sud-
denly those pressures drop, there wont 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 isnt 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 encephalopa-
thy.

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 <90 over the
next couple of months. Again, no first line medication is currently recommended.

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CARDIOGENIC SHOCK
Introduction
Shock is a state characterized by decreased perfusion and decreased oxygenation of
tissues. This will cause disruption at the cellular level. If caught early, all of the damage
will be reversible, but over time, will lead to cell death, organ failure, and eventually
death.
Cardiogenic shock stems from the heart not being able to pump normally.

Etiology
The etiology will be anything that causes the heart to stop pumping eciently, but will usu-
ally occur from an MI.

Signs and Symptoms


Classically, they will behypotensive, altered,and havecool clammy skin. Ultimately meta-
bolic acidosis develops. Systemic vascular resistance and heart rate will be increased.
Look for chest pain and dyspnea in someone with a history of cardiac disease. There will
also be pulmonary congestion and elevated cardiac enzymes.

Treatment
Always stabilize the patient before trying to attempt to find an etiology. This means aggres-
sive fluid resuscitation, followed by pressors (norepinephrine or dopamine) if needed.

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ORTHOSTATIC HYPOTENSION
Introduction
This usually occurs because of autonomic dysfunction and is an inadequate physiological
response to postural changes. This will usuall occur in patients over the age of 65.

Etiology
Medications, hypovolemia, anemia, heart disease, diabetes, and or Parkinsons disease.

Signs and Symptoms


When the patient suddenly stands, they will feel dizzy, have palpitations, and become syn-
copal.

Diagnostic Testing
Take the blood pressure lying down, then have the patient stand for a couple minutes,
and then repeat the blood pressure. The diagnosis is made if the systolic blood pressure
falls 20mmHg or if the diastolic falls 10mmHg or more. Order tilt table testing if suspicion
is high, but orthostatic vital signs are normal.

Treatment
Treat the underlying etiology. If none is found, attempt to increase fluid and sodium
intake. If no response, give fludrocortisone (mineralcorticoid) as first line medical therapy.

ATRIAL FIBRILLATION/FLUTTER
Introduction
Atrial fibrillation is the most common cardiac arrhythmia. Fibrillation can be thought of as

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a worsening of flutter. These patients are at increased risk for stroke due to the potential
for thrombus formation. This is because of the constant quivering from the atria. The
blood will become stagnant and a clot will form. It takes a couple of days after atrial fibril-
lation starts, for a thrombus to form.

Signs and Symptoms


Both types may present with palpitations, shortness of breath, and/or chest pain.

Diagnostic Testing
Diagnosed on ECG. Fibrillation will have an irregularly irregular rhythm without any P
waves. Atrial flutter will present as a regular rhythm with a saw tooth pattern. Flutter will
usually have an atrial rate of 300 and a ventricular rate of 150.

Treatment
Unstable patients are treated the same:
Cardioversion

If this is the first episode, order an echocardiogram to evaluate for thrombus formation.
Trans esophageal echo is more sensitive than trans thoracic. If the patient has been
symptomatic for less than two days, you may rate control or cardiovert (may be safely
done because it is too soon for a thrombus to form). If symptoms have been present for
more than 2 days, then the possibility of thrombus exists, and ideally you want to rate
control (beta blockers or calcium channel blockers) as the first line option. If a calcium
channel blocker is used, use the non dihyropyridines (verapamil or diltiazem).

If the patient requests cardioversion and symptoms have been present over 2 days, order
an echo to rule out a thrombus. If no thrombus exists, give heparin and cardiovert. If the
echo shows a thrombus, you must anticoagulate with warfarin for four weeks before car-
dioverting.

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Finally, make sure you provide long term anticoagulation with either aspirin or warfarin.
So, when do we use warfarin and when do we use aspirin? CHADS2 score:

C-CHF (1point)
H-Hypertension (1point)
A-Age of 75 (1point)
D-Diabetes (1point)
S-Stroke or TIA in past (2 points given here)

Score:
0: Aspirin
1: Aspirin or warfarin
2: warfarin

HEART BLOCK

First Degree Long PR Interval (>.20) No Treatment

PR progressively lengthens, No treatment if patient is asymptomatic.


Mobitz 1/Wenckebach 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 2 Mobitz 1, however, no
lengthening of the PR is noted.
May present with syncope

Signal from the atria does not


reach the ventricle. Therefore,
Third Degree
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 aected. Wide QRS (over .12), notched R wave in V5 and V6. ST and T waves dis-
placement 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 ar-
rhythmia 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 sig-
nal 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 dierent 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 dierentiate between SVT or aberrant conduction. Always treat a wide complex
tachycardia as ventricular tachycardia. If unstable, cadiovert. If stable treat with ami-
dorone 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 poly-
morphic ventricular tachycardia.

Treatment: withdraw the oending drugs, correct electrolyte abnormalities, and cardiac
pacing. Magnesium sulfate may be oered 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 patients 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 ad-
junct 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 en-
zymes 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 excep-
tions:

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.

PhysicianAssistantBoards.com Andrew Reid PA-C 22


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 oered 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 in-
terscapular back pain.

Diagnostic Testing
AAA is diagnosed on ultrasound. Dissection may have a blood pressure dierential be-
tween 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.

PhysicianAssistantBoards.com Andrew Reid PA-C 23


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, al-
lowing 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 pre-
sent 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 resultsto start the prednisone if GCA is suspected.

PhysicianAssistantBoards.com Andrew Reid PA-C 24


SYSTOLIC MURMURS

Usually seen in the


Systolic
elderly due to Patients who
The most common crescendo-
calcification of the present with any
symptoms include decrescendo
aorta. The other symptoms need
dyspnea, angina, murmur. Heard
Aortic Stenosis two etiologies surgical correction
dizziness. Patients best at the second
include congenital immediately due to
may also present right intercostal
bicuspid/unicuspid the high risk of
with syncope. space radiating to
valve and sudden death.
the neck.
rheumatic disease

Heard best at the Treatment is with


left upper sternal balloon valvotomy.
dyspnea, fatigue,
Pulmonic Stenosis border and may If severe, then
and syncope.
have ejection click. surgery is
indicated.

Asymptomatic
patients are not
treated. Those with
Patients are usually symptoms are
Murmur:
The main etiology asymptomatic, but given vasodilators.
holosystolic
is mitral valve may have dyspnea If severe,
Mitral Regurgitation murmur. Heard
prolapse and and fatigue. worsening, or no
best over apex and
coronary disease. improvement in
radiates to axilla.
symptoms with
medications, the
next step Is
surgery.
Murmur: Has a
This is usually
mid-systolic click,
asymptomatic, but
with a possible late
may cause chest
Mitral Valve systolic murmur
pain, palpitations, Beta Blockers
Prolapse depending on the
and anxiety.
severity of
Usually present in
regurgitation
women
present.
Murmur: Diuretics are used
Symptoms are non-
holosystolic for symptoms. For
specific, might be
Most commonly murmur. Heard those with heart
those of right sided
Tricuspid from dilation of best left mid sternal failure, therapy
heart failure if
Regurgitation right atrium and border. When should be aimed at
present.
ventricle regurgitation is that. For severe
severe, the murmur disease, surgery is
will fade. performed.
25
DIASTOLIC MURMURS

Treatment is with
Dilation of aortic Asymptomatic. Blowing quality.
surgery for those
root or congenital Will present with Will become
who are
bicuspid valve. wide pulse holosystolic as the
Aortic symptomatic, or
Outside the US the pressure (water regurgitation
Regurgitation those with
most common hammer pulse). worsens. Heard
progressive
cause is rheumatic best at the left
enlargement if
disease sternal border.
asymptomatic.

Decrescendo
Pulmonic Pulmonic murmur. Identical
Regurgitation hypertension to aortic
regurgitation.
Shortness of
Treatment is with
breath. Pregnancy
balloon valvotomy
will exacerbate
Low pitch rumble. or surgery.
symptoms, or
Mitral Stenosis Rheumatic disease Best heard at the Diuretics and beta
cause initial
apex. blockers may be
symptoms in those
used for symptom
who were
control only.
asymptomatic
Ace inhibitors and
Heard best at 4th diuretics may be
Rheumatic
Symptoms are intercostal space used for symptom
disease. Will
Tricuspid Stenosis similar to other at the lower left control. If no
occur with other
valvular disorders. sternal border. improvement
valve abnormality
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 diag-
nosed 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
benet for the treatment of PAD.

PhysicianAssistantBoards.com Andrew Reid PA-C 26


PHLEBITIS/THROMBOPHLEBITIS

This is a thrombus in a superficial vein, most commonly the saphenous vein, causing in-
flammation 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 hospitaliza-
tion, and/or immobilization. A small percent will not have risk factors and are termed un-
provoked DVT.

Signs and Symptoms


The patient will present with unilateral lower extremity pain, erythema, and swelling. Ho-
man 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).

27
PhysicianAssistantBoards.com Andrew Reid PA-C
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 eect. 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 arent 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 aect mur-
mur 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.

PhysicianAssistantBoards.com Andrew Reid PA-C 28


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

Usually seen in the


Patients who present
elderly due to The most common Systolic crescendo-
with any symptoms
calcification of the symptoms include decrescendo
need surgical
aorta. The other two dyspnea, angina, murmur. Heard best
Aortic Stenosis correction
etiologies include dizziness. Patients at the second right
immediately due to
congenital biscupid/ may also present intercostal space
the risk of sudden
unicuspid valve and with syncope. radiating to the neck.
death.
rheumatic disease

Heard best at the left Treatment is with


Dyspnea, fatigue, upper sternal border balloon valvotomy. If
Pulmonic Stenosis
and syncope and may have severe, surgery
ejection click indicated.

Asymptomatic
patients arent
treated. Those with
The main etiology is
Asymptomatic. May Holosystolic murmur symptoms are given
mitral valve prolapse
Mitral Regurgitation have dyspnea and heard best over apex vasodilators. If
and coronary
fatigue and radiates to axilla severe, worsening,
disease
or no improvement
with meds, the next
step is surgery.

Asymptomatic. But,
Mid systolic click
may cause
with possible late
palpitations, chest Treat with beta
Mitral Valve Prolapse systolic murmur
pain, and anxiety. blockers
depending on the
Usually present in
severity
women.

Holosystolic murmur Diuretics for


Symptoms are non
heard best left mid symptoms. Those
Most commonly from specific. Symptoms
Tricuspid sternal border. with heart failure
dilation of right can be the same as
Regurgitation When regurgitation treat accordingly.
atrium and ventricle right sided heart
is sever, murmur will Surgery in severe
failure
fade. disease. 29
Diastolic Murmurs

Treatment is with
Blowing quality. Will
Dilation of aortic surgery for those
Asymptomatic. Will become
root or congenital who are
present with wide holosystolic as the
bicuspid valve. symptomatic, or
pulse pressure regurgitation
Aortic Regurgitation Outside the US the those with
(water hammer worsens. Heard
most common progressive
pulse). best at the left
cause is rheumatic enlargement if
sternal border.
disease asymptomatic.

Decrescendo
Pulmonic
Pulmonic murmur. Identical to
hypertension
Regurgiation aortic regurgitation.

Shortness of
Treatment is with
breath. Pregnancy
balloon valvotomy
will exacerbate
Low pitch rumble. or surgery.
symptoms, or
Rheumatic disease Best heard at the Diuretics and beta
Mitral Stenosis cause initial
apex. blockers may be
symptoms in those
used for symptom
who were
control only.
asymptomatic

Ace inhibitors and


diuretics may be
Rheumatic disease. Heard best at 4th
Symptoms are used for symptom
Will occur with intercostal space at
similar to other control. If no
Tricuspid Stenosis other valve the lower left
valvular disorders improvement
abnormality sternal border
balloon valvotomy
or surgery is done

PhysicianAssistantBoards.com Andrew Reid PA-C 30


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 us-
ers (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

PhysicianAssistantBoards.com Andrew Reid PA-C 31


History of endocarditis
Prosthetic valves
Unrepaired cyanotic congenital heart disease.
Cardiac transplant patients

AND are undergoing:

Dental procedures that aect 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 diuse 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 eusion and will not have wall motion abnormalities.

PhysicianAssistantBoards.com Andrew Reid PA-C 32


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, mued 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 eusion and chamber collapse. Definitive
diagnosis and treatment is done with pericardiocentesis.

PhysicianAssistantBoards.com Andrew Reid PA-C 33


REVIEW QUESTIONS

1. How will the ejection fraction dier 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 dierence 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?

PhysicianAssistantBoards.com Andrew Reid PA-C 34


17.What will happen if a patient who presents with WPW is accidentally given adeno-
sine?

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 dierentiate 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 bi-
opsy?

26.What is the only medication with proven benefit in peripheral artery disease?

27.What is the most common vein aected in patients with superficial thrombophlebi-
tis?

28.What are risk factors for DVT?

29.When should a D-Dimer be ordered for DVT?

30.How does respiration aect 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?

PhysicianAssistantBoards.com Andrew Reid PA-C 35


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?

PhysicianAssistantBoards.com Andrew Reid PA-C 36


Review Answers

1.How will the ejection fraction dier 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 ejec-
tion 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. Spiranolac-
tone 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 CON-
TRAINDICATED 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.

PhysicianAssistantBoards.com Andrew Reid PA-C 37


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 cya-
nosis. 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 ventri-
cle 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 re-
versal 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 other-
wise healthy?
Diuretics, ACE/ARBs, or Amlodipine (long acting dihydropyridine).

14.What is the dierence between hypertension urgency and emergency?


They will both have a blood pressure >180/120. The dierence is that
hypertension emergency will also have end organ damage.

PhysicianAssistantBoards.com Andrew Reid PA-C 38


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 dierentiate unstable angina from NSTEMI?


Both will clinically present the same. Both will have similar EKG findings. The only
dierence 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 sus-
picion is high, continue to monitor for 12 hours. The most specific cardiac marker

PhysicianAssistantBoards.com Andrew Reid PA-C 39


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 screen-
ing 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 aected in patients with superficial thrombo-
phlebitis?
Saphenous vein

28.What are risk factors for DVT?


Know Virchows triad: hypercoagulability, stasis, and endothelial injury. If risk fac-
tors are not present, this is termed unprovoked DVT.

PhysicianAssistantBoards.com Andrew Reid PA-C 40


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 sus-
pected, this should never be ordered. DVT has a high sensitivity, but horrible speci-
ficity. This means many things can elevate the value, but it is almost always ele-
vated in patients with DVT. Remember, only order if the clinical suspicion is low.

30.How does respiration aect murmurs?


Inspiration will increase right sided murmurs. Expiration will increase left sided mur-
murs. 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 as-
sociated 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 col-
lected. 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?


Diuse ST elevations with PR depression. An MI will have ST elevations, but they
will not be diuse.

PhysicianAssistantBoards.com Andrew Reid PA-C 41


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, mued heart sounds, and distended neck veins.

PhysicianAssistantBoards.com Andrew Reid PA-C 42


QUICK FACTS/ASSOCIATIONS

CONDITION FACT/ASSOCIATION

Orthopnea, paroxysmal nocturnal dyspnea,


CHF
jugular venous distention, S3

HOCM Sudden death in athlete

Atrial Septal
Fixed wide splitting of S2
Defect

Coarctation of
X-Ray: Rib notching, 3 sign
Aorta

PDA Machine like murmur

Tetralogy of
Cyanosis with crying or feeding
Fallot

VSD Holosystolic murmur

Cardiogenic
Hypotensive, cool, clammy skin
Shock

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
Independent P wave and QRS complex
Block

Paroxysmal
Supraventricular Narrow complex tachycardia
Tachycardia

Stable Angina Chest pain relieved with rest

PhysicianAssistantBoards.com
Andrew Reid PA-C 43
CONDITION FACT/ASSOCIATION

Diffuse ST segment elevations, coronary


Prinzmetal Angina
artery spasm

ACS Morpine, oxygen, nitrates, aspirin

Cocaine Induced
NO betablockers, give benzodiazepines
MI

Aortic Aneurysm Tobacco

Marfan Syndrome, Ehlers-Danlos


Aortic Dissection syndrome, tearing chest pain, Wide
mediastinum

Jaw claudicaton, visual disturbance, >50


GCA
years of age

PAD Leg pain relieved with rest, cilastazol

Superficial
Palpable Cord
Thrombophlebitis

Virchows triad, unilateral LE swelling, pain,


DVT
and erythema. Homan sign

Right side murmurs increase with


Murmurs inspiration. Left side murmurs increase with
expiration

Systolic, second right intercostal space,


Aortic Stenosis radiates to neck

Mitral regurgitation Holosystolic murumur

MVP Women, anxiety, mid-systolic click

Aortic
Wide pulse pressure. Water hammer pulse
Regurgitation

New murmur, fever, injection drug use,


Endocarditis streptococcus viridans , Jane way lesions,
Osler nodes, Roth spots
Pleuritic chest pain. Worse upon laying,
Pericarditis improves with sitting. ST segment
elevation, PR depression

PhysicianAssistantBoards.com Andrew Reid PA-C 44


Condition Facts/Associations

Becks triad (hypotension,


muffled heard sounds,
Cardiac Tamponade distended neck vein),
pulses paradoxus, electrical
alternans.

PhysicianAssistantBoards.com Andrew Reid PA-C 45