ROSH REVIEW ALL UPDATED ACTUAL Questions and CORRECT Answers
1. What side effects of glucocorticoid treat- Osteoporosis, glucose intolerance, and hy-
ment should be monitored for in patients pertension.
with polymyalgia rheumatica?
2. What medications may cause pupillary di- Antihistamines, asthma medications, adren-
lation and increase the risk of an episode ergics, anticholinergics, and tricyclic antide-
of acute angle-closure glaucoma? pressants.
3. What is the most common type of fistula Colovesical fistula
that can form in patients with acute diver-
ticulitis?
4. True or false: A prostate specific antigen True
level of zero guarantees the absence of
prostate cancer?
5. A 63-year-old man presents to the clinic C
concerned about his upcoming ski vaca-
tion. The last time he vacationed in the High altitude illness is caused by the hypox-
mountains three years ago, he developed ic effects of a rapid ascent in altitude (typ-
high altitude pulmonary edema. He is ically greater than 3000 meters). The term
wanting to discuss what measures he can encompasses several syndromes including
take to prevent this from occurring again. acute mountain sickness (AMS), high altitude
In addition to advising he ascend grad- pulmonary edema (HAPE), and high altitude
ually, which of the following is recom- cerebral edema (HACE). HAPE manifests two
mended for prevention of high altitude to four days after a rapid ascent and is the
pulmonary edema? most common cause of death among the
high altitude illnesses. Symptoms include a
A Acetazolamide dry cough progressing to dyspnea at rest.
B Dexamethasone Pulse oximetry reveals saturation values at
C Nifedipine least 10 points lower than expected, and val-
D Sildenafil ues may be as low as 40 to 50%. Physi-
cal examination findings include low-grade
, fever, tachycardia, tachypnea, and inspiratory
crackles. Approaches to prevent HAPE include
gradual ascent, preacclimatization, avoidance
of alcohol, and pharmacologic prophylaxis
with nifedipine in patients at high risk. Those
considered high risk include individuals with
a history of HAPE or HACE, history of AMS
and ascending to 2800 m or higher in less
than two days, ascending > 500 m/day above
3000 m without extra days for acclimatization,
ascending > 3500 m in less than two days,
and comorbid conditions predisposing to al-
titude illness.
Acetazolamide (A) is the mainstay of pharma-
cologic prevention of acute mountain sick-
ness (AMS) and high altitude cerebral edema
(HACE). It is also the recommended first-line
drug treatment for mild AMS. Dexametha-
sone (B) is recommended as an alternative
to acetazolamide in the prevention of AMS
and HACE. It is also used as a first-line drug
treatment for moderate to severe AMS and
HACE. Sildenafil (D) is being investigated for
prevention of high altitude pulmonary ede-
ma (HAPE), but its use is not currently recom-
mended.
6. What are symptoms of acute mountain Fatigue, anorexia, nausea, vomiting,
sickness? headache, insomnia, dizziness, and short-
ness of breath with exertion.
,7. What is the Beck triad of cardiac tampon- Hypotension, jugular venous distention, and
ade? muffled heart sounds
8. In patients with relatively large atrial sep- Cardiac enlargement and increased pul-
tal defects, what findings would be evi- monary vascularity
dent on chest radiography?
9. What is a VSD murmur A ventricular septal defect (C) causes a thrill
at the left lower sternal border, a holosystolic
murmur, and a loud single S2 in severe cases.
This may often be referred to as a Still mur-
mur.
10. A 26-year-old woman presents to the clin- C
ic with a six-month history of dilated car-
diomyopathy. Her twin sister suffered a Dilated cardiomyopathy is characterized by
sudden cardiac death six months ago and impaired contraction and dilation of one or
was diagnosed with dilated cardiomyopa- both ventricles, and is the most common di-
thy postmortem. This patient was subse- agnosis in patients referred for cardiac trans-
quently evaluated and discovered to have plantation. Most patients present between
the condition and cardiac phenotype test- the ages of 20-60 years. The most com-
ing was performed. She denies chest mon clinical manifestations are symptoms
pain, dyspnea on exertion, presyncope, of heart failure (orthopnea, paroxysmal noc-
palpitations, or edema. Recent echocar- turnal dyspnea, peripheral edema, and im-
diogram reveals a dilated left ventricle paired exercise capacity). Other presenta-
with an ejection fraction of 45%. Which of tions include coexisting dysrhythmia, throm-
the following therapies is the next step in boembolic complications, incidental detec-
management of this patient? tion of asymptomatic cardiomegaly, and sud-
den death. Even though dilated cardiomy-
Amloidpine opathy may be caused by a variety of infec-
Furosemide tious, toxic, or metabolic agents, frequent-
ICD device ly no etiology can be found. It is con-
Left atrial appendage occlusion sidered idiopathic if other causes, such as
, coronary artery disease and myocarditis, are
excluded by thorough evaluation, includ-
ing coronary angiography, echocardiogra-
phy, and endomyocardial biopsy when indi-
cated. Family-based studies that include clin-
ical screening of first-degree family mem-
bers have established that a significant num-
ber of patients diagnosed with idiopathic di-
lated cardiomyopathy have familial dilated
cardiomyopathy. Most familial dilated car-
diomyopathy is transmitted in an autosomal
dominant pattern, although all inheritance
patterns have been recognized. Given the
frequency of familial dilated cardiomyopathy,
all new cases of idiopathic dilated cardiomy-
opathy should undergo evaluation, including
consideration of molecular genetic testing.
Medical therapy is based on cardiac pheno-
type. In addition, an implantable cardiovert-
er-defibrillator should be considered in pa-
tients with a family history of sudden cardiac
death, even if the ejection fraction is greater
than 35% (the usual threshold for prophylac-
tic placement).
Amlodipine (A) is a calcium channel block-
er that demonstrated no benefit nor harm
when used in patients with class II or III heart
failure. Furosemide (B) is the most com-
monly used loop diuretic in the treatment of
heart failure. This patient is not demonstrat-
ing symptoms of heart failure, so this is not
1. What side effects of glucocorticoid treat- Osteoporosis, glucose intolerance, and hy-
ment should be monitored for in patients pertension.
with polymyalgia rheumatica?
2. What medications may cause pupillary di- Antihistamines, asthma medications, adren-
lation and increase the risk of an episode ergics, anticholinergics, and tricyclic antide-
of acute angle-closure glaucoma? pressants.
3. What is the most common type of fistula Colovesical fistula
that can form in patients with acute diver-
ticulitis?
4. True or false: A prostate specific antigen True
level of zero guarantees the absence of
prostate cancer?
5. A 63-year-old man presents to the clinic C
concerned about his upcoming ski vaca-
tion. The last time he vacationed in the High altitude illness is caused by the hypox-
mountains three years ago, he developed ic effects of a rapid ascent in altitude (typ-
high altitude pulmonary edema. He is ically greater than 3000 meters). The term
wanting to discuss what measures he can encompasses several syndromes including
take to prevent this from occurring again. acute mountain sickness (AMS), high altitude
In addition to advising he ascend grad- pulmonary edema (HAPE), and high altitude
ually, which of the following is recom- cerebral edema (HACE). HAPE manifests two
mended for prevention of high altitude to four days after a rapid ascent and is the
pulmonary edema? most common cause of death among the
high altitude illnesses. Symptoms include a
A Acetazolamide dry cough progressing to dyspnea at rest.
B Dexamethasone Pulse oximetry reveals saturation values at
C Nifedipine least 10 points lower than expected, and val-
D Sildenafil ues may be as low as 40 to 50%. Physi-
cal examination findings include low-grade
, fever, tachycardia, tachypnea, and inspiratory
crackles. Approaches to prevent HAPE include
gradual ascent, preacclimatization, avoidance
of alcohol, and pharmacologic prophylaxis
with nifedipine in patients at high risk. Those
considered high risk include individuals with
a history of HAPE or HACE, history of AMS
and ascending to 2800 m or higher in less
than two days, ascending > 500 m/day above
3000 m without extra days for acclimatization,
ascending > 3500 m in less than two days,
and comorbid conditions predisposing to al-
titude illness.
Acetazolamide (A) is the mainstay of pharma-
cologic prevention of acute mountain sick-
ness (AMS) and high altitude cerebral edema
(HACE). It is also the recommended first-line
drug treatment for mild AMS. Dexametha-
sone (B) is recommended as an alternative
to acetazolamide in the prevention of AMS
and HACE. It is also used as a first-line drug
treatment for moderate to severe AMS and
HACE. Sildenafil (D) is being investigated for
prevention of high altitude pulmonary ede-
ma (HAPE), but its use is not currently recom-
mended.
6. What are symptoms of acute mountain Fatigue, anorexia, nausea, vomiting,
sickness? headache, insomnia, dizziness, and short-
ness of breath with exertion.
,7. What is the Beck triad of cardiac tampon- Hypotension, jugular venous distention, and
ade? muffled heart sounds
8. In patients with relatively large atrial sep- Cardiac enlargement and increased pul-
tal defects, what findings would be evi- monary vascularity
dent on chest radiography?
9. What is a VSD murmur A ventricular septal defect (C) causes a thrill
at the left lower sternal border, a holosystolic
murmur, and a loud single S2 in severe cases.
This may often be referred to as a Still mur-
mur.
10. A 26-year-old woman presents to the clin- C
ic with a six-month history of dilated car-
diomyopathy. Her twin sister suffered a Dilated cardiomyopathy is characterized by
sudden cardiac death six months ago and impaired contraction and dilation of one or
was diagnosed with dilated cardiomyopa- both ventricles, and is the most common di-
thy postmortem. This patient was subse- agnosis in patients referred for cardiac trans-
quently evaluated and discovered to have plantation. Most patients present between
the condition and cardiac phenotype test- the ages of 20-60 years. The most com-
ing was performed. She denies chest mon clinical manifestations are symptoms
pain, dyspnea on exertion, presyncope, of heart failure (orthopnea, paroxysmal noc-
palpitations, or edema. Recent echocar- turnal dyspnea, peripheral edema, and im-
diogram reveals a dilated left ventricle paired exercise capacity). Other presenta-
with an ejection fraction of 45%. Which of tions include coexisting dysrhythmia, throm-
the following therapies is the next step in boembolic complications, incidental detec-
management of this patient? tion of asymptomatic cardiomegaly, and sud-
den death. Even though dilated cardiomy-
Amloidpine opathy may be caused by a variety of infec-
Furosemide tious, toxic, or metabolic agents, frequent-
ICD device ly no etiology can be found. It is con-
Left atrial appendage occlusion sidered idiopathic if other causes, such as
, coronary artery disease and myocarditis, are
excluded by thorough evaluation, includ-
ing coronary angiography, echocardiogra-
phy, and endomyocardial biopsy when indi-
cated. Family-based studies that include clin-
ical screening of first-degree family mem-
bers have established that a significant num-
ber of patients diagnosed with idiopathic di-
lated cardiomyopathy have familial dilated
cardiomyopathy. Most familial dilated car-
diomyopathy is transmitted in an autosomal
dominant pattern, although all inheritance
patterns have been recognized. Given the
frequency of familial dilated cardiomyopathy,
all new cases of idiopathic dilated cardiomy-
opathy should undergo evaluation, including
consideration of molecular genetic testing.
Medical therapy is based on cardiac pheno-
type. In addition, an implantable cardiovert-
er-defibrillator should be considered in pa-
tients with a family history of sudden cardiac
death, even if the ejection fraction is greater
than 35% (the usual threshold for prophylac-
tic placement).
Amlodipine (A) is a calcium channel block-
er that demonstrated no benefit nor harm
when used in patients with class II or III heart
failure. Furosemide (B) is the most com-
monly used loop diuretic in the treatment of
heart failure. This patient is not demonstrat-
ing symptoms of heart failure, so this is not
