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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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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;
<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 definition 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, hypertrophic 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
Dilated
Ventricle is dilated,
leading to decreased
contraction of the
ventricle
Systolic
Same as CHF
Hypertrophic
Normal or impaired
ventricular filling with
ventricular hypertrophy
and preserved systolic
function.
Diastolic
Beta Blockers, followed
by Calcium Channel
Blockers.
Restrictive
Impaired ventricular
filling without
hypertrophy of the
ventricle. Also has
impaired contractility. This is the least
common cause of
cardiomyopathy in the
states.
Diastolic dysfunction,
which can lead to
systolic dysfunction
No specific Treatment
available
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 children 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
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The best test for diagnosis is an echocardiogram. The ASD will usually close spontaneously, 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 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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Andrew Reid PA-C 11
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 <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 efficiently, but will usually occur from an MI. Signs and Symptoms
Classically, they will be hypotensive, altered, and have cool clammy skin. Ultimately metabolic 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 aggressive 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 Parkinson’s disease.
Signs and Symptoms
When the patient suddenly stands, they will feel dizzy, have palpitations, and become syncopal.
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 fibrillation 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 cardioverting.
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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
Mobitz 1/Wenckebach
Mobitz 2
Third Degree
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Long PR Interval (>.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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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 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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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, 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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Andrew Reid PA-C 24
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.
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Andrew Reid PA-C
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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). PhysicianAssistantBoards.com
Andrew Reid PA-C
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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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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
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
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 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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Andrew Reid PA-C 31
•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. 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, 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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Andrew Reid PA-C 33
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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Andrew Reid PA-C 34
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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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?
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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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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 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.
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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 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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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 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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Andrew Reid PA-C
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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
PhysicianAssistantBoards.com
Andrew Reid PA-C
44
Condition
Facts/Associations
Cardiac Tamponade
Becks triad (hypotension,
muffled heard sounds,
distended neck vein),
pulses paradoxus, electrical
alternans.
PhysicianAssistantBoards.com
Andrew Reid PA-C
45