This document provides a practice question sample set for the medical licensing exam preparation platform Osmosis. It includes two sample questions, one testing basic science knowledge of myocardial infarction histology, and the other testing diagnosis of Dressler Syndrome, a post-myocardial infarction condition. The basic science question asks which histological elements would be found on microscopic examination of a patient's heart tissue given autopsy findings and timeline. The diagnosis question presents a patient presenting 8 weeks after a myocardial infarction with fever, sore throat, shortness of breath and back pain to test recognition of Dressler Syndrome.

1. Jeremiah Pamer, DO
6/19/2016
jeremiahpamer@gmail.com
303.880.5664
Practice question sample set for Osmosis
#1. Basic Science Question
Theme: Cardiovascular
Pathophysiology Tested: Myocardial infarction and the timeline of macroscopic elements
associated with light microscopy evaluation of myocardium histology
A 55 year old African American Male who is obese and in obvious distress presents to the
Emergency Department after driving himself from work with a chief complaint of chest pain. It
began 45 minutes ago and the pain is described as substernal pressure with intermittent
electrical shooting pains down his left arm and into his jaw that has been intermittent. He has a
past medical history of Type II Diabetes, hypertension, hyperlipidemia, and sickle cell trait. His
medications include Metformin, Pravastatin, Lisinopril and Hydrochlorothiazide. Family history is
pertinent for his father having had two “heart attacks.”
An ECG is performed and is shown below.
https://upload.wikimedia.org/wikipedia/commons/2/2d/Inferior_and_RtV_MI_with_PVC_15_lead.
jpg

2. Physical Examination is pertinent for dilated pupils bilaterally, no jugular venous distension
noted and there are accessory muscle utilized with every respiration. The heart has no audible
rubs, murmurs or bruits heard upon auscultation and has a regular rhythm, with S1 and S2
noted. The lungs are clear in all fields bilaterally upon auscultation. There are no abdominal
bruits via auscultation. Femoral, Posterior Tibial and Dorsal Pedis arterial pulses are 2+
bilaterally.
Laboratory results include a troponin of 1.4 ng/ml. All other laboratory findings were within
normal limits.
Despite comprehensive resuscitation efforts the patient dies before he can be taken to the cath
lab for percutaneous cardiac intervention.
An autopsy was performed and the following illustration is a reliable facsimile of what the
patient’s heart tissue looked like macroscopically.

3. https://en.wikipedia.org/wiki/Myocardial_infarction#/media/File:Heart_ant_wall_infarction.jpg
Which of the following sets of histological elements are most likely to be found with microscopic
examination of the patient’s myocardium?
A. Glycogen Depletion, as seen with a PAS Stain and waviness of fibers at border
Incorrect:​ This description is most indicative of early light microscopy findings after
myocardial infarction; 4­12 hours post MI. While the cells on the edge of the injury may
demonstrate the components of Answer A, it is not the best answer.
B. Ongoing coagulation necrosis, karyopyknosis, hypereosinophilia of myocytes,
contraction band necrosis in margins and the beginning of neutrophil infiltration
Correct:​ See Main explanation below
C. Beginning of disintegration of dead muscle fibers, necrosis of neutrophils, beginning of
macrophage removal of dead cells at border
Incorrect:​ (Beginning of disintegration of dead muscle fibers, necrosis of neutrophils,
beginning of macrophage removal of dead cells at border.) These elements speak to an
infarction event much earlier than 12­24 hours prior to death, and in this case is
categorized as 3­7 days post MI. There is no evidence of disintegration of tissue, or
macrophage involvement, which usually occurs 7­10 days post infarction.
D. Increased collagen deposition, decreased cellularity
Incorrect:​ Of all the possible answers, this description would place the myocardial
infarction the furthest away from this patient’s death. The elements of this answer occur
between 2­8 weeks post injury.
Main Explanation: ​This question describes a patient who had a massive coronary infarction, as
demonstrated by his chief complaint, past medical and family history, physical exam, ECG and
troponin levels. This is a histological pathology question that requires you to know the
histological findings of myocardium in various time frames after initial infarction. While this
patient’s description of having this pain for only 45 minutes may seem like a large clue, it is
actually more of a red­herring in that the troponin levels are extraordinarily elevated and would

4. not be seen in this short of time frame, as troponin is indicative of myocardial necrosis.
Furthermore, atypical chest pain can manifest in ambiguous symptoms, and the patient’s
confession of not feeling well for weeks immediately prior could mean that he has had
numerous small infarctions.
The largest piece of evidence used to correctly evaluate this question is the image of the heart
during dissection. The heart tissue demonstrates that an infarction episode occurred earlier than
the immediate hours before his death, but within 24 hours of his death. In the initial 4 hours after
a myocardial infarction there is no change with light histology evaluation of myocardium, but it
should be noted that electron microscopy may show mitochondrial swelling, relaxed myofibrils
and glycogen depletion. The consistent dark mottling, coagulation necrosis, and other elements
of Answer B make this the best answer. Also, troponin levels following MI peak between 18­24
hours post infarction, and the severely elevated troponin levels seen with this patient point
toward the time frame inherent with the correct answer.
Major Takeaway:
Light microscopy and histological evaluation of myocardial tissue after an infarction involves a
process over time that is important to know to properly identify when the injury happened to the
heart upon autopsy. The principles behind the initial injury and subsequent changes seen in the
next 2 months are actually quite simple, and with a satisfactory understanding of inflammatory
immune agents and when they are involved, the correct answer can be reached reliably.
This table may help summarize the time frames and changes seen.
Time Gross examination Histopathology
(light microscopy)
0 ­ 0.5 hours None None

5. 0.5 – 4 hours None* ● Glycogen Depletion, as seen with
a PAS Stain
● Possibly waviness of fibers at
border
4 – 12 hours ● Sometimes
dark ​mottling
● Initiation of ​coagulation necrosis
● Edema
● Hemorrhage
12 – 24 hours ● Dark mottling ● Ongoing coagulation necrosis
● Karyopyknosis
● Hypereosinophilia​ of myocytes
● Contraction band necrosis​ in
margins
● Beginning of ​neutrophil​ infiltration
1 – 3 days ● Infarct center
becomes
yellow­​tan
● Continued coagulation necrosis
● Loss of nuclei and ​striations
● Increased infiltration of
neutrophils to ​interstitium
3 – 7 days ● Hyperemia​ at
border
● Softening
yellow­tan
center
● Beginning of disintegration of
dead muscle fibers
● Necrosis of neutrophils
● Beginning of ​macrophage
removal of dead cells at border
7 – 10 days ● Maximally soft
and yellow­tan
● Red­tan
margins
● Increased phagocytosis of dead
cells at border

6. ● Beginning of ​granulation tissue
formation at margins
10 – 14 days ● Red­gray and
depressed
borders
● Mature granulation tissue with
type I collagen​[1]
2 – 8 weeks ● Gray­white
granulation
tissue
● Increased collagen deposition
● Decreased cellularity
More than 2
months
Completed scarring Dense collagenous scar formed
https://en.wikipedia.org/wiki/Timeline_of_myocardial_infarction_pathology
References:
● Bishop JE, Greenbaum R, Gibson DG, Yacoub M, Laurent GJ. Enhanced deposition of
predominantly type I collagen in myocardial disease. J Mol Cell Cardiol.
1990;22:1157–1165
● Rangogiannis NG: The immune system and cardiac repair. Pharmacol Res. 2008, 58:
88­111
● Campobasso CP, Dell’Erba AS, Addante A, Zotti F, Marzullo A, Colonna MF: Sudden
cardiac death and myocardial ischemia indicators: a comparative study of four
immunohistochemical markers. Am J Forensic Med Pathol. 2008, 29: 154­161.
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#2. Diagnosis Question
Theme: Cardiovascular
Disease Diagnosis Tested: Myocardial Infarction and diagnosis of the postmyocardial
infarction syndrome, also known as Dressler Syndrome

7. A moderately distressed 76 year old male presents to your ambulatory clinic for a follow up
appointment from a myocardial infarction that was diagnosed in the Emergency Department 8
weeks ago. He had significantly elevated troponin II levels and dramatically elevated ST
segments in lead II, III and aVF. He now complains of fever, a sore throat, shortness of breath
and a sharp pain that radiates to the inferior portion of his left scapula, all of which suddenly
came on 3 days prior. The patient states he assumed he was getting a cold. He is a member of
a religious organization which prohibits blood transfusions, and due to the risk of needing a
transfusion refused to undergo percutaneous cardiac intervention while in the Emergency
Department and left the hospital the next day. The patient has no significant medical history
prior to having an MI. He has been prescribed numerous medications in the past 8 weeks, but
sheepishly admits to not taking them regularly. He has continued to smoke 2 packs/day and
drink ¼ bottle of whisky every day since his myocardial infarction, just as he has done for the
previous 60 years.
Physical examination demonstrates:
Body System Pertinent Physical Exam Finding
CV Significant Jugular Venous Distension, Regular rate and rhythm, with positive
rub heard at all cardiac listening posts, no bruits or murmurs.
Resp Crackles heard upon auscultation in bilateral lower lung fields
Abd 3x5 cm pulsatile mass felt left of midline deep in the abdomen
GU Positive stool guaiac test
Which of the following best describes the nature of the most likely diagnosis of the his patient?
A. A disease state frequently characterized by a ​Staphylococcus aureus ​mediated
endocarditis involving the tricuspid valve
Incorrect: ​This describes an infective endocarditis secondary to intravenous drug
abuse, which is overwhelmingly associated with tricuspid involved endocarditis. More
than half of the IV drug abuse endocarditis diagnoses identify ​Staphylococcus aureus​ as

8. the causative agent. While this patient does heavily drink and smoke, no mention of IV
drug abuse is mentioned, but it certainly is not completely out of the question. However,
it is not the best answer, as postmyocardial infarction syndrome (Dressler Syndrome) is
much more likely in the setting of a non­reperfusion infarction injury.
B. A viral infection of the heart muscle cells that can lead to dilated cardiomyopathy and
death
Incorrect:​ It is unlikely this patient has a viral myocarditis when the symptoms and
medical history point to a postmyocardial infarction syndrome (Dressler Syndrome) as
being much more likely. The stem of the question does qualify this with stating the
patient felt like he may have a cold, but don’t let this fool you into choosing viral
myocarditis as the best answer.
C. A disease pathology that involves a robust autoimmune response secondary to
neo­antigens related to tissue injury that may result in fibrinous pericarditis
Correct: See Main Explanation below
D. This diagnosis is highly associated with smoking and surgical intervention is generally
indicated for a lesion that is >5.5cm in males
Incorrect: ​This describes an Abdominal Aortic Aneurysm (AAA), which this patient is at
high risk for, especially as a pulsatile mass was palpated deep in the midline of the
abdomen. This patient does warrant an evaluation for a AAA (first with ultrasound and
then with CT scan, if indicated) and if the physical exam was correct, he very well may
have an indication for surgical intervention. However, even though this is the 2nd best
answer, it is not the best answer compared to postmyocardial infarction syndrome
(Dressler Syndrome)
Main Explanation:
Postmyocardial infarction syndrome (Dressler Syndrome) is an autoimmune response
secondary to a variety of injuries to the heart and surrounding tissue. Specifically, it is thought
that there are new antigens (neo­antigens) that are from the necrotic and fibrous tissue in the
injured myocardium that trigger this autoimmune response. This diagnosis has actually

9. decreased in incidence in recent years; this is thought to be with the dramatic increase of
percutaneous cardiac intervention procedures which allow for reperfusion of the injured tissue.
The patient in the vignette elected to forgo the catheter lab due to religious reasons, however, it
should be noted that the most common reason for a patient not receiving percutaneous cardiac
intervention is distance from a major medical center with a cath lab.
The best treatment option for postmyocardial infarction syndrome is high dose aspirin, and in
some refractory cases, corticosteroids. NSAIDs are to be avoided in patients with coronary
artery disease, in general, and this disease as well.
Major Takeaway:
Postmyocardial infarction syndrome (Dressler Syndrome)​ should be on the differential in
any patient who is post cardiac injury (infarction, surgery, PCI) and presents with chest pain,
especially pericardial type symptoms. While the overall incidence has decreased, in patients
with non­reperfusion myocardial infarction clinical courses the risk is much higher. First line
treatment is high dose aspirin, NSAIDs should be avoided.
References:
● Hutchcroft BJ. Dressler’s syndrome. ​British Medical Journal​. 1972;3(5817):49.
● Lawrence MS, Wright R. Tamponade in Dressler's syndrome with immunological
studies. ​Br Med J.​1972 Mar 11;1(5801):665–666.
● Shahar, A, Hod, H, Barabash, G, et al Disappearance of a syndrome: Dressler’s
syndrome in the era of thrombolysis.Cardiology85,255­258.
● Fever after acute myocardial infarction: Dressler's syndrome demonstrated on cardiac
MRIVan Kolen, K. et al., International Journal of Cardiology , Volume 183 , 209 ­ 210
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#3. Management Question
Theme: Cardiovascular

10. Management Principle Tested: ​Recognizing Torsades de pointes and identifying the best first
treatment option
A 33 year old female is brought to the Emergency Department by police for threatening tourists
with cannibalistic intent and multiple syncopal episodes witnessed by the police. She is
delusional and gaining any information from the patient is futile. However, she has a medical
record that shows frequent psychiatric hospitalizations and a prescription for lithium, among
other antipsychotics. She is hemodynamically stable upon presentation, and remains so until
she has another witnessed syncopal episode. She is breathing and has a palpable peripheral
pulse. An ECG is done at this time, this is what it shows:
https://upload.wikimedia.org/wikipedia/commons/a/a5/Torsades_de_Pointes_TdP.png
Which of the following best represents the first line management option at this time?
A. Call a code blue and initiate 3 person CPR with a bag mask
Incorrect:​ A code blue is a very common code for cardiopulmonary arrest. It is obvious
that this patient is not in cardiopulmonary arrest, as she is breathing and has a palpable
pulse. Never initiate CPR on a patient with pulses and who is breathing.
B. Call a code blue and attempt synchronized cardioversion
Incorrect: ​A code blue is a very common code for cardiopulmonary arrest. It is obvious
that this patient is not in cardiopulmonary arrest, as she is breathing and has a palpable
pulse. However, the other element of this answer must be considered with a little more
thought. While it is a good idea to place pacer pads on the patient and have a
pacer/defibrillator on hand in this setting, this question specifically calls for ​synchronized

11. cardioversion​. The ECG demonstrates no clear QRS complex. A synchronized
cardioversion is programmed to apply current during the peak of the R wave.
C. Get a stat lithium toxicology blood test and initiate fluid therapy with normal saline
Incorrect:​ It is possible that this patient has a lithium overdose, however, the police nor
the clinical staff has witnessed symptoms associated with elevated lithium overdose,
other than torsades de pointes (TDP.) Regardless, the acute medical issue that
demands immediate action is the TDP seen on the 12 lead ECG. While the best therapy
for lithium overdose is high levels of sodium given intravenously, normal saline would
most likely be given in the setting of her repeated syncopal episodes. To further clarify,
we are not given vital signs for this patient which may indicate the need for fluid therapy
such as hypotension and tachycardia, so it is not known whether this patient should be
treated with normal saline fluid thereapy.
D. Administer magnesium sulfate via intravascular push
Correct:​ Magnesium sulfate is the first line antiarrhythmic treatment for torsades de
pointes (TDP). The ECG clearly demonstrates TDP, and if there was any doubt, the
documented prescription for lithium allows for secondary evidence that TDP is the
diagnosis.
Main Explanation:
Torsades de pointes (TDP) ​is an acute cardiac rhythm that can lead to ventricular fibrillation
and sudden cardiac death. Symptoms associated with TDP include palpitations, dizziness,
syncopal episodes which are usually short lived, as most instances of TDP auto­convert to sinus
rhythm within 5 seconds of onset. The patient in this question unquestionably has TDP as
indicated via the ECG and answering this question correctly relies mainly on knowing that
magnesium sulfate is first line treatment for TDP. However, answers A and B can be ruled out in
that this patient is clearly not in cardiopulmonary arrest in that she is breathing and there are
palpable pulses. Even if you are not familiar with what a “code blue” involves, the other
components of these answers should still allow you to rule out them as candidates for the
correct answer. Breathing for someone in the way of using a bag mask is inappropriate in that
the patient is still breathing, and in answer B, synchronized cardioversion is not first line
treatment in TDP.
TDP has a number of causes, the most common being electrolyte imbalances, including
hypomagnesemia, hypokalemia and hypocalcemia, and prescription drug interactions and
side­effect profiles that include prolonged QT syndrome, which is a potential precursor of TDP.
First line treatment is magnesium sulfate.
Major Takeaway:
Torsades de pointes (TDP)​ is a dangerous cardiac rhythm that can easily lead to sudden
cardiac death. It has a broad etiology, but the most common reasons are electrolyte imbalances
(low potassium and/or magnesium), prescription drug interactions, such as clarithromycin,
levofloxacin, haloperidol and lithium, and also there are congenital causes for prolonged QT

12. syndrome. First line treatment is administration of magnesium sulfate via IV. Other
antiarrhythmics are 2nd line treatment.
​References:
● Tzivoni, D, Keren, A, Chenzbraun, A, Gottielb, J, Benhorin, J, Stem, S. Efficacy of
MgSO4 in torsade de pointes: report on two patients (abstr). ​Isr J Med Sci​. 1983;19:398.
● Beach, Scott R. et al., QTc Prolongation, Torsades de Pointes, and Psychotropic
Medications. Psychosomatics , Volume 54 , Issue 1 , 1 ­ 13
● Del Gobbo LC, Imamura F, Wu JH, et al. Circulating and dietary magnesium and risk of
cardiovascular disease; a systematic review and meta­analysis of prospective studies.
Am J Clin Nutr 2013; 98:160