Key Answers of Part 2 December 2019 - Nabeel Ibrahim Page 1

KEY ANSWERS
OF
PART 2 EXAM
DECEMBER 2019

ARAB BOARD IN INTERNAL MEDICINE

DECEMBER 2021
BAGHDAD

Key Answers of Part 2 December 2019 - Nabeel Ibrahim Page 2

These are NOT the formal answers, and are NOT necessarily true.

1. B. Hypoxic-ischemic encephalopathy. The outcome of RSE is often

poor. The risk of mortality with RSE is mainly associated with the
underlying etiology and is increased with hypoxic encephalopathy and
brain tumors. (UpToDate).
2. B. Immune Reconstriction Inflammatory Syndrome. IRIS due to
preexisting infection with JC virus — HIV-infected patients co-infected
with JC virus may develop progressive multifocal leukoencephalopathy
(PML) after CD4 cell counts drop below 200/microL. Although some
HIV-infected patients with PML improve following the initiation of
ART, about 10 to 20 percent of patients may develop new or worsening
neurologic symptoms associated with enlarging CNS lesions that show
secondary enhancement after infusion of contrast agents (a finding not
typically present in AIDS patients with PML). It can be challenging
clinically to distinguish PML disease progression from PML IRIS.
(Collazos J, Mayo J, Martínez E, Blanco MS. Contrast-enhancing
progressive multifocal leukoencephalopathy as an immune reconstitution
event in AIDS patients. AIDS 1999; 13:1426.).
3. A. A clearly delineated hypodense lesion in the left middle cerebral
artery territory. Amarican Academy of Neurology recommeded that
thrombolytic is contraindicated if more than one third of MCA territory
infarction is present. (AAN).
4. B. A 48-year-old man with no medical history who presents with calf
pain following prolonged air travel. The D-dimer measured by
enzyme-linked immunosorbent assay (ELISA) is elevated in the
setting of breakdown of fibrin by plasmin, and the presence of a
positive D-dimer can prompt the need for additional imaging for
deep venous thrombosis and/or pulmonary embolus in specific
clinical situations where the patient would be considered to have
an elevation in D-dimer. However, one must be cautious about
placing value on an elevated D-dimer in other situations where
there can be an alternative explanation for the elevated level. Of
the scenarios listed in the question, the only patient who would be
Key Answers of Part 2 December 2019 - Nabeel Ibrahim Page 3
 expected to have a negative D-dimer would be the patient with
calf pain and recent air travel. The presence of a normal alveolar-
arterial oxygen gradient cannot reliably differentiate between those
with and without pulmonary embolism. In all the other scenarios,
elevations in D-dimer could be related to other medical conditions
and provide no diagnostic information to inform the clinician
regarding the need for further evaluation. Some common clinical
situations in which the Ddimer is elevated include sepsis,
myocardial infarction, cancer, pneumonia, the postoperative state,
and the second and third trimesters of pregnancy. (Reference:
Harrison's Principles of Internal Medicine Self-Assessment and Board
Review, 19th Edition).
5. A. Liver biopsy or fibroscan is recommended. Assessment of liver
disease severity is necessary prior to therapy. Diagnosing clinically
inapparent cirrhosis (METAVIR score F4) or advanced (bridging)
fibrosis (METAVIR score F3) is required, as the choice of treatment
regimen and the post-treatment prognosis and surveillance for HCC
every 6 months depend on the stage of fibrosis. Patients with cirrhosis
need to be assessed for portal hypertension, including oesophageal
varices.
6. B. Chronic Respiratory Acidosis. (References: OnExamination Part 1).
7. E. Transient Vertebrobasilar Ischemia. The clinical symptomatology
is strongly suggestive of "drop attacks" resulting from transient ischemia
in the vertebrobasilar territory. Ischemia of the pyramidal tract in the
brainstem is the most probable pathogenetic mechanism. Transient
ischemic attacks (TIAS), by definition, last less than 24 hours (usually
less than 1 hour). TIA is often a harbinger of stroke, especially when
involving the carotid circulation. Adverse drug reaction (choice A) must
be considered as a potential etiology of frequent falls in an elderly
patient, especially when hypotension is the suspected mechanism and
there is a history of antihypertensive medication. The most common
adverse effect of alendronate is esophagitis. Lateral medullary infarction
(choice B) follows occlusion of the vertebral or posterior inferior
cerebellar artery. Its manifestations include ataxia, vertigo, nystagmus,
impaired pain and temperature sensation on the ipsilateral face and
contralateral body, dysphagia, and hoarseness. Parkinson disease (choice
Key Answers of Part 2 December 2019 - Nabeel Ibrahim Page 4
 C) leads to resting tremor, rigidity, and bradykinesia. Falls due to
Parkinson disease result from loss of postural reflexes, which can be
assessed by the pull-test. Postural hypotension (choice D) is a frequent
cause of falls in the elderly and is often the result of medication.
Typically, the patient reports a light-headed sensation on standing or
getting up from bed, and the fall may be accompanied by a transiently
obtunded consciousness. The carotid bruit in this case is probably
secondary to atherosclerotic stenosis of the carotid artery but not to the
patient's symptoms. Transient ischemia in the carotid territory (choice E)
manifests with motor deficits, sensory symptoms, or alterations in
language expression or comprehension (aphasia). (Reference: Kaplan
USMLE Step 2 CK Qbook 2008-2009).
8. C. Corona virus.
9. E. High Resolution CT Scan of the chest.
10. C. Organophosphate posisoning.
11. D. The severity of paraneoplastic syndrome is not related to
tumor bulk. Horner syndrome refers to the triad of miosis, ipsilateral
ptosis and lack of facial sweating. It is caused by infiltration of the
sympathetic chain and stellate ganglion by lung cancer (i.e. intrathoracic,
not extrathoracic, spread). Cushing syndrome may be the result of
ectopic production of adrenocorticotropic hormone by small cell lung
cancer. Clinical manifestations include weakness, muscle wasting,
drowsiness, confusion, dependent oedema, moon facies, hypertension,
hypokalaemic alkalosis, and hyperglycaemia. Lambert-Eaton myasthenic
syndrome (LEMS) is characterised by gradual onset of proximal lower
extremity weakness while proximal upper extremity weakness is usually
less noticeable. Improvement of muscular strength with repeated testing
is a distinctive symptom of LEMS and muscular weakness may improve
during the day. The severity of the symptoms is not correlated with the
tumour bulk. Even very small cancers may produce paraneoplastic
syndromes. Typical paraneoplastic syndromes such as LEMS, stiff man
syndrome or Cushing syndrome warrant a search for a tumour.
(Reference: European Respiratory Society | Self-Assessment in
Respiratory Medicine Q99 [MODIFIED]).
12. D. Treatment should include levofloxacin.
13. B. Eye exam is required.
14. B. Give rifampin and doxycycline for 6 weeks.

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15. C. Intubation and mechanical ventilation.
16. C. Lower incidence of dyskinesias. DAs have intermediate potency
for improving motor symptoms and have a lower risk of motor
complications than levodopa; however, they carry a higher risk of
somnolence, hallucinations, and impulse control disorders (ICDs), and
they are not well tolerated in older adults and those with cognitive
dysfunction.
17. D. Low thyroid stimulating hormone level.
18. A. Lacunar infarction of the internal capsule. Pure motor loss is
usually due to a lacunar infarct. (Reference: Crash Course - Neurology
4th edition).
19. A. Graves's disease.
20. B. Propylthiouracil.
21. E. Lifestyle counseling and start insulin. Metformin monotherapy is
not helpful in improving symptoms in this setting, because the initial
dose is low and increased over several weeks. Insulin, rather than oral
hypoglycemic agents, is often indicated for initial treatment of
symptomatic or severe hyperglycemia:
 fasting plasma glucose >250 mg/dL [13.9 mmol/L],
 random glucose consistently >300 mg/dL [16.7 mmol/L], or
 A1C >10 [85.8 mmol/mol]
22. E. Repeat CT adrenal study after 6-12 months.
23. A. Morning spot urine for albumin/creatinine. The management of
glomerulopathy due to diabetes mellitus is a common and important task
that all general internists must face. In the United States, diabetes is the
leading cause of end-stage renal disease (ESRD). It occurs in 33% of all
diabetics. Diabetic nephropathy is a spectrum of progressive renal
disease ranging from microalbuminuria (30–300 mg/24 h) to overt
nephrotic syndrome and ESRD. In terms of incidence, 30 to 40% of type
I diabetics and 15 to 20% of type II diabetics will acquire ESRD in 20
years. So how does one screen for diabetic nephropathy and try to
prevent its progression? Urine dipsticks that are commonly found at
internists' offices are not sensitive enough to detect microalbuminuria
and will only be positive once the albumin level is above 300 mg. The
collection of timed urine samples is required for the diagnosis of early

Key Answers of Part 2 December 2019 - Nabeel Ibrahim Page 6

 nephropathy. One way of collecting is the 24-hour urine for
microalbumin. However, there are wide variations in the amount of
albumin that is excreted in that period of time. Upright posture, protein
ingestion, and exercise all tend to increase urine albumin excretion. For
all these reasons, a more accurate method to detect microalbuminuria is
to do a morning spot urine for albumin/creatinine. Patients should be
instructed to discard a voided urine sample before going to bed and then
collecting urine samples thereafter until the morning. When the value is
30 to 300 mg albumin per gram of creatinine, microalbuminuria is
present. The prevention of the progression of diabetic nephropathy once
it is found can be accomplished by tight glycemic control, a low protein
diet (0.8 g/kg/day), and initiation of angiotensin-converting enzyme
(ACE) inhibitors. ACE inhibitors have been found to slow the
progression of proteinuria, even in normotensive diabetics. This patient's
glycemic control is nearly optimal and should be maintained to keep the
HgbA1c approximately 7.0% by weight loss, as well as adjusting the
insulin regimen. Although all these measures will be beneficial in
reducing proteinuria, a diagnosis first needs to be made. (Reference:
Kaplan Internal Medicine Question Book).
24. B. Acute allograft rejection.
25. B. Implantable Cardiovertor Defibrillator. Torsades de pointes
refer to ventricular tachycardia (VT) that is characterized by
polymorphic QRS complexes that change in amplitude and cycle length,
giving the appearance of oscillations around the baseline. This rhythm is
associated with QT prolongation. For patients with congenital,
prolonged, QT-interval syndrome, beta-adrenergic blocking agents have
been the mainstay of therapy. Implantable cardioverter/defibrillators
(ICDS) with dual- chambered pacing capability have become the
treatment of choice for patients with recurrent episodes despite beta
blockers. ICD devices have been developed that will promptly recognize
and terminate life-threatening ventricular arrhythmias. Clinical trials
testing the function of these devices in patients with drug-refractory
ventricular arrhythmias have demonstrated survival from sudden death at
1 year ranging between 92 and 100%. Currently, ICDS should be
considered for patients with VT that is not hemodynamically tolerated.
Key Answers of Part 2 December 2019 - Nabeel Ibrahim Page 7
 This is either if the VT occurs spontaneously, resulting in syncope or
sudden death, or at induction in the laboratory with the development of
symptoms. ICDS are also useful for patients with spontaneous, sustained
VT and depressed, electrophysiological study is an indication for ICD
placement if there is evidence or coronary artery disease, left ventricular
dysfunction, or a prior infarction. Cervicothoracic sympathectomy has
been proposed as a form of therapy for congenital prolonged QT
syndrome, but it is not often effective as the sole therapy. Some
investigators have used pacing in combination with sympathectomy
when beta blockers fail, but it is not uniformly successful and can result
in Horner's syndrome. Class IA agents such as quinidine may induce QT
prolongation and so is contraindicated for patient with prolonged QT
syndrome. left ventricular function. Sustained or nonsustained VT at
26. C. Plasmapheresis. This patient presents with familial
hypercholesterolemia (FH), which is a common autosomal dominant
disorder due to absent or defective LDL receptors and resulting in a
decreased capacity to remove plasma LDL. LDL cholesterol levels are
markedly increased. It is associated with characteristic xanthomas in the
Achilles, patellar, and extensor tendons of the hands and by the presence
of xanthelasma. Corneal arcus is frequently seen. It is frequently
associated with early coronary artery disease (CAD), peripheral vascular
disease, and cerebral vascular disease. The plasma cholesterol level is
generally in the range of 300 to 500 mg/dL, and in some patients
homozygous for FH, it can exceed 800 to 1,000 mg/dL. Triglyceride
levels are usually normal, but in 10% of patients, they may be mildly
elevated. Because of the risk of CAD, these patients need especially
vigorous therapy. A low-fat and low-cholesterol diet should be initiated,
although it gives only a moderate result and will not be enough to
control the problem by itself. Effective therapy can be achieved with
HMG-CoA reductase inhibitors (statins) as first-line therapy. They lower
LDL by 20 to 45%. When they are combined with a bile acid-binding
resin, levels of LDL may be decreased by 50 to 60%. In some patients,
triple therapy with a statin, a bile acid-binding resin, and niacin may be
necessary. Patients homozygous for FH may not be responsive to these
measures. For them, measures such as plasmapheresis or LDL apheresis
Key Answers of Part 2 December 2019 - Nabeel Ibrahim Page 8
 are indicated. Liver transplant is the last resort when all else fails as
treatment.This patient is already on maximum doses of statins and bile
acid-binding agent. The addition of niacin did not help. There is very
little chance that any additional medical therapy will solve this patient’s
problem; that is why plasmapheresis is indicated. (Reference: Kaplan
Internal Medicine Question Book).
27. B. Hyperosmolar Non_ketotic Coma.
28. E. Right paramedian branch of the basilar artery. Foville
Syndrome. Inferior medial pontine syndrome, also known as Foville
syndrome, is one of the brainstem stroke syndromes occurring when
there is infarction of the medial inferior aspect of the pons due to
occlusion of the paramedian branches of the basilar artery. This
infarction involves the following:
 corticospinal tract: contralateral hemiplegia/hemiparesis
 medial lemniscus: contralateral loss of proprioception and
vibration
 middle cerebellar peduncle: ipsilateral ataxia
 facial nerve (CN VII) nucleus: ipsilateral facial weakness
 abducens nerve (CN VI) nucleus: lateral gaze paralysis
and diplopia
Clinical presentation: The presentation can be variable but manifests
usually as a gaze palsy to the side of the lesion, ipsilateral abducens, and
ipsilateral facial palsy and contralateral hemiplegia may be present.
Crossed hemihypesthesia and ipsilateral cerebellar signs may be present
in the more complete form.
The Posterior Cerebral Artery (PCA) supplies the occipital lobe, the
inferior part of the temporal lobe, and various deep structures including
the thalamus and the posterior limb of the internal capsule.
The superior cerebellar artery supplies deep parts and superior parts of
the of the cerebellum. It supples parts of the midbrain (tectum, including
the cerebral crus). It also supplies superior medullary velum, the superior
cerebellar peduncle, the middle cerebellar peduncle, and the
interpeduncular region.

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 The short circumferential arteries are branches of the P1 or P2 segments
of PCA that ascend along the lateral surface of the mesencephalon,
supplying the tegmentum of midbrain and the base of the peduncle.
29. C. Measure urinary catecholamines. For the patient described, the
markedly increased calcitonin level indicates the diagnosis of medullary
carcinoma of the thyroid. In view of the family history, the patient most
likely has multiple endocrine neoplasia (MEN) type 2A, which includes
medullary carcinoma of the thyroid gland, pheochromocytoma, and
parathyroid hyperplasia. Pheochromocytoma may exist without
sustained hypertension, as indicated by excessive urinary catecholamine
metabolites. Before thyroid surgery is performed on this patient, a
pheochromocytoma must be ruled out through urinary metanephrine
determinations; the presence of such a tumor might expose him to a
hypertensive crisis during surgery. The serum calcium serves as a
screening test for hyperparathyroidism. At surgery, the entire thyroid
gland must be removed because foci of parafollicular cell hyperplasia, a
premalignant lesion, may be scattered throughout the gland. Successful
removal of the medullary carcinoma can be monitored with serum
calcitonin levels. Medullary carcinoma of the thyroid rarely metastases
to the liver, so a liver scan would be unnecessary if liver enzymes are
normal. Thyroxine will be needed after surgery, but MEN type 2 is not
associated with hypothyroidism. Radioactive iodine can be used to treat
malignancies that arise from the follicular cells of the thyroid;
parafollicular cells, however, do not take up iodine and do not respond to
radioactive iodine. Hyperparathyroidism, while unlikely in this
eucalcemic patient, is probably present in his brother. (Reference:
PreTest Medicine 14e).
30. D. Repeat echocardiography in 6 months.
31. D. Initiate liraglutide.
32. A. Barium esophagraphy.
33. C. No further testing. Educational Objective: Evaluate preoperative
cardiac risk using electrocardiography in a patient with known
cardiovascular disease. The most appropriate preoperative cardiac testing
for this patient is electrocardiography (ECG). The 2014 American
College of Cardiology/American Heart Association guideline on
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 perioperative cardiovascular evaluation and management of patients
undergoing noncardiac surgery states that preoperative ECG is
reasonable for patients with known atherosclerotic cardiovascular
disease (including coronary artery disease, arrhythmia, peripheral artery
disease, cerebrovascular disease, or significant structural heart disease)
who are undergoing CONT moderate- to high-risk surgeries.
Preoperative ECG also may be considered for other asymptomatic
patients, except for those undergoing low-risk procedures. This patient
has known coronary artery disease and has not undergone ECG in 2
years. It is reasonable to obtain ECG preoperatively because certain
interval findings (for example, new Q waves), additional evidence of
conduction disease, or arrhythmia may result in changes in perioperative
management. Risk calculators, including the Revised Cardiac Risk Index
and the American College of Surgeons National Surgical Quality
Improvement Program myocardial infarction and cardiac arrest
calculator, can be used to determine the risk for a perioperative major
adverse cardiac event (MACE). Patients with low risk (<1% risk for
perioperative MACE) may proceed to surgery without preoperative
cardiac stress testing. whereas patients with elevated risk (?.1% risk for
perioperative MACE) should undergo assessment of functional capacity.
Metabolic equivalents (METs) are used to represent the patient's
functional capacity based on the intensity of activity able to be
performed. If the patient's functional capacity exceeds 4 METs, the
patient may proceed to surgery without further testing. Examples of 4
METs of activity include the ability to walk 4 miles per hour on a flat
surface, climb one to two flights of stairs without stopping, or perform
vigorous housework such as vacuuming. Swimming for 30 minutes also
exceeds this threshold. Cardiac stress testing should generally be
reserved for patients at elevated risk for MACE with a functional
capacity less than 4 METs, but only if the results of the test will change
perioperative management. Although this patient has an elevated risk for
a MACE perioperatively, his functional capacity exceeds 4 METs;
therefore, he does not require preoperative cardiac stress testing with
dobutamine or exercise. Preoperative electrocardiography is reasonable
for patients with known atherosclerotic cardiovascular disease, including
Key Answers of Part 2 December 2019 - Nabeel Ibrahim Page 11
 coronary artery disease, arrhythmia, peripheral artery disease,
cerebrovascular disease, or significant structural heart disease, who are
undergoing moderate- to high-risk surgeries; cardiac stress testing should
generally be reserved for patients at elevated risk for major adverse
cardiac event with a functional capacity less than 4 metabolic
equivalents. but only if the results of the test will change perioperative
management. (Reference: Modified MKSAP18 General Internal
Medicine Question, Q34).
34. A. Actigraphy. Educational Objective: Evaluate a patient with
excessive day time sleepiness with actigraphy. The most appropriate
management is testing with actigraphy. The initial step in the evaluation
of the patient with excessive daytime sleepiness is to ensure adequate
quantities (7 io 8 hours) of sleep on a regular basis. This patient's self-
report of a variable bedtime and restricted sleep schedule during the
workweek raises the possibility of insufficient sleep syndrome. Wrist
actigraphy measures movement and ambient light to estimate nightly
sleep periods during a 1 to 2 week time frame. Actigraphy is more
accurate than patient reports of sleep duration and is likely more accurate
than sleep diaries. When actigraphy isn't available, a sleep diary can be a
useful alternative. Insufficient sleep syndrome suggested by either
actigraphy or sleep diary should prompt a trial of sleep extension.
Modafinil is a stimulant medication used in hypersomnia syndromes
such as narcolepsy. It would not be appropriate therapy without first
excluding insufficient sleep syndrome. Multiple sleep latency testing can
be useful in the evaluation of pathologic daytime sleepiness (for
example, narcolepsy) and may help establish a diagnosis of narcolepsy,
but it is resource intensive and expensive. It should be performed only
after addressing insufficient sleep quantities and polysomnography has
ruled out common sleep disorders such as sleep apnea.
Polysomnography or home sleep testing would be indicated if the
clinical history strongly suggested a primary sleep disorder such as
obstructive sleep apnea. However, obstructive sleep apnea is unlikely in
a young woman who is not overweight and does not have obvious upper
airway abnormalities. In addition, the patient is suspected of having a
restricted sleep schedule that should be evaluated first with actigraphy.
Key Answers of Part 2 December 2019 - Nabeel Ibrahim Page 12
 KEY POINT: The initial step in the evaluation of the patient with
excessive daytime sleepiness is to ensure adequate quantities of sleep on
a regular basis using either actigraphy or a sleep diary. (Reference:
MKSAP18 Pulmonary and Critical Care Medicine, Q72).
35. E. Acute fatty liver of pregnancy.
36. C. Belimumab. Educational Objective: Treat refractory systemic
lupus erythematosus with belimumab. Belimumab is the most
appropriate therapeutic option to consider in this patient with a history of
systemic lupus erythematosus (SLE) who continues to have active
disease manifestations primarily affecting the skin and joints while she is
on appropriate standard immunosuppressive therapy, including
glucocorticoids. She has not been able to tolerate other
immunosuppressive agents commonly used to treat active disease
manifestations. Therefore, an alternative approach or escalation of the
therapy is appropriate for this patient. Belimumab is FDA approved as
an addition to standard therapy in patients who have SLE with mild to
moderately active disease. Belimumab is designed to inhibit B-
lymphocyte stimulator (BLyS) protein. BLyS plays a key role in the
selection, maturation, and survival of B cells, and it has a significant role
in the pathogenesis of SLE. The addition of belimumab to standard
therapy reduces disease activity levels and delays flares in patients with
serologically active SLE or prior glucocorticoid use. Its use is also
associated with improved quality of life in appropriately selected
patients. Belimumab has been found to be most effective in patients with
mucocutaneous and joint manifestations; its role in other disease
manifestations continues to be studied and evolve. Abatacept is a T-cell
costimulatory inhibitor that has been tried in SLE but not found to be
effective. Adalimumab is a tumor necrosis factor (TNF)-a inhibitor
effective in the treatment of rheumatoid arthritis and spondyloarthritis.
Blocking TNF in patients with SLE has not been effective and may
potentially worsen the disease. The interleukin (]L)-17 inhibitor
secukinumab is' an approved therapy for psoriatic arthritis and
ankylosing spondylitis. The role ofIL-17 and its blockade in SLE is
under investigation but is currently not well elucidated in SLE.
Secukinumab has not been studied in SLE and is not an appropriate
Key Answers of Part 2 December 2019 - Nabeel Ibrahim Page 13
 therapy. KEY POINT: Belimumab is FDA approved as an addition to
standard therapy in patients who have systemic lupus erythematosus
with persistent mild to moderately active disease. (Reference:
MKSAP18 Rheumatology Q90).
37. D. A-a gradient more than 15 mm Hg.
38. E. 100 mL/hr.
39. C. Entrapment neuropathy of the left lateral femoral cutaneous
nerve. This patient is experiencing meralgia paresthetica—an
entrapment neuropathy of the lateral femoral cutaneous nerve. Risk
factors include abdominal obesity and tightfitting belts/corsets. Diabetic
amyotrophy (Answer A) is a lumbosacral plexopathy that occurs in
diabetic patients even with good blood sugar control. It causes pain,
weakness, and muscle atrophy of the anterior thigh. Avascular necrosis
(AVN) and degenerative arthritis (osteoarthritis) of the hip joint usually
localizes as pain in the groin or deep buttock. Hip range of motion is
often impaired. Trochanteric bursitis (Answer D) causes pain overlying
the trochanteric bursa at the lateral hip. It does not impair passive hip
range of motion, but it is not associated with paresthesias or numbness.
(Reference: THE BRIGHAM INTENSIVE REVIEW OF INTERNAL
MEDICINE QUESTION AND ANSWER COMPANION).
40. E. High-dose insulin therapy. Calcium-channel blocker overdose is
associated with substantial morbidity and mortality. The effects of
overdose depend on the type and dose of calcium channel blocker. In
addition to vasodilation and decreased inotropy, diltiazem and
verapamil, but not the dihydropyridines, typically result in bradycardia.
Recognition of the overdose is important, as hemodynamic deterioration
can be delayed by hours after the ingestion. In addition to supportive and
symptomatic care, treatment usually includes intrave- nous calcium and
glucagon. Whole bowel irrigation may be appropriate for ingestion of
extended-release preparations. Temporary pacemaker support may be
indicated for persistent bradycardia. High-dose insulin therapy has been
increasingly advocated for cases of calcium-channel blocker (and beta-
blocker) overdose [Intensive Care Med. 2007;33:2019–24]. The
mechanisms of action are unclear, but calcium channel blockers may
cause insulin resistance in the myocardium that is overcome by high
Key Answers of Part 2 December 2019 - Nabeel Ibrahim Page 14
 doses of insulin. While this therapy is usually instituted with a
concomitant glucose infusion, calcium channel blocker overdose itself
can cause impaired glucose metabolism, and patients are often
hyperglycemic and may not require additional glucose. Recently, another
treatment, intravenous lipid emulsion, has been advocated for use in
several types of severe overdoses, including calcium-channel blocker
overdose [J Intensive Care Med. 2012; June 24]. While this therapy has
not been well studied, results from animal studies and case reports of
severe toxicity in humans have demonstrated evidence of benefit. The
mechanism of action is unclear, but it may work by acting as a "lipid
sink" for the toxic medication. Hemodialysis is not effective for
removing verapamil because verapamil is highly protein bound (Answer
A). Bicarbonate infusion may be indicated in the setting of severe
academia or a widened QRS complex due to sodium channel blockade,
as in tricyclic overdose (Answer B). Physostigmine is a therapy for
anticholinergic overdose (Answer D). Intravenous corticosteroids are not
helpful in calcium-channel blocker overdose (Answer E). (Reference:
THE BRIGHAM INTENSIVE REVIEW OF INTERNAL MEDICINE
QUESTION AND ANSWER COMPANION 2014).
41. E. Prednisone. Glucocorticoids – Systemic glucocorticoids are used
to gain control of the disease in patients with significant illness or
systemic involvement. Most patients with hypocomplementemia require
this therapy to achieve control of the illness. The dosing of
glucocorticoids varies and is usually dictated by the severity of systemic
illness. We begin treatment at doses between 0.5 and 1 mg/kg per day or
equivalent. Benefits from glucocorticoids are usually noticeable within a
day or two of initiation. We typically give these medications for at least
a week before making an assessment about clinical response. Rarely, a
patient may require glucocorticoid doses of 1.5 mg/kg per day.
Typically, once control of disease is established, the dose of
glucocorticoids is gradually reduced week by week to the lowest dose
that will control the disease. Some patients can be tapered off
glucocorticoid therapy over time, although many cannot and require
protracted use. Because of the long-term sequelae of glucocorticoids,
glucocorticoid-sparing therapies should be considered in such patients
Key Answers of Part 2 December 2019 - Nabeel Ibrahim Page 15
 and efforts made to find adjunctive treatments that might allow for
lowering of the chronic glucocorticoid dose.
42. C. Polymyositis.
43. C. Start LMWH and admit.
44. C. Catheter ablation. This patient is experiencing supraventricular
tachycardia as a result of previous repair of tetralogy of Fallot. Tetralogy
of Fallot is the most common form of cyanotic congenital heart disease
after 1 year of age, with an incidence approaching 10% of all forms of
congenital heart disease. The defect is due to anterocephalad deviation of
the outlet septum, resulting in four possible features: (1) ventricular
septal defect, (2) overriding aorta, (3) pulmonary valve stenosis, and (4)
consequent right ventricular hypertrophy. To reach adulthood, most
patients will have had surgery, either palliative, or more commonly,
reparative. A few patients, however, will present as adults with an
uncorrected tetralogy of Fallot. Natural survival into the fourth decade is
rare (approximately 3%) After intracardiac repair, over 85% of patients
are asymptomatic on follow-up. Palpitations from atrial and ventricular
tachycardias, with or without dizziness or syncope, and dyspnea from
progressive right ventricular dilation secondary to chronic pulmonary
regurgitation occur in 10 to 15% of patients at 20 years after initial
repair. Physical examination may reveal a parasternal right ventricular
lift from right ventricular dilation. Ventricular tachycardia can arise at
the site of the right ventriculotomy, from ventricular septal defect (VSD)
patch suture lines, or from the right ventricular outflow tract. Recurrent
episodes of supraventricular tachycardia will eventually require catheter
ablation of the site of reentry to terminate this patient’s dysrhythmias.
Verapamil and amiodarone can worsen the rhythm disturbance.
(Reference: Kaplan Internal Medicine Question Book).
45. B. Diffuse Proliferative GN. This is a case of Henoch–Schönlein
purpura (HSP). Diffuse proliferative GN is characterized by acute
nephritic syndrome: AKI over days to weeks, with hypertension,
edema, oliguria, and active urine sediment. Less severe clinical
presentation correlates with a more benign biopsy. The pattern of
glomerular involvement is similar to IgA nephropathy. (Fauci,
Chapter 277). (Reference: Lange Q & A INTERNAL MEDICINE 5e.).
Key Answers of Part 2 December 2019 - Nabeel Ibrahim Page 16
46. B. Oxidation of Fe2+ to Fe3+.
47. C. Repeat blood smear every 8 hours for 3 days. The recent travel
history to a malaria-endemic region, and especially the sequential
occurrence of typical febrile attacks every other day, should alert the
physician to the possibility of Plasmodium infection. This parasite
should be looked for in peripheral blood smears. Thick blood films are
used for detection, whereas thin blood films are used for identification of
the Plasmodium species. The number of parasites varies considerably
during the course of the disease, and Plasmodium falciparum (the most
dangerous species) is particularly difficult to detect. Thus, to establish
the diagnosis, blood smears should be examined every 8 hours during
and between febrile attacks for at least 3 days. Blood cultures (choice A)
are not useful in this case since Plasmodium parasites cannot be cultured.
An ELISA test for P. falciparum has recently become available.
Repeating blood smears during an attack (choice C) or just once (choice
D) may not be sufficient to demonstrate Plasmodium parasites in red
blood cells. Starting treatment with chloroquine (choice E) before
establishing diagnosis is not appropriate, although chloroquine is the
agent of choice for prophylaxis and therapy of malaria. However,
chloroquine-resistant strains of P. falciparum are present throughout the
world, including Africa. Patients with falciparum malaria should be
hospitalized. In addition, before starting treatment for acute malaria, it is
essential to establish whether the patient has received any other
antimalarial medication in the previous days to avoid the risk of
overdose. (Reference: Kaplan Step 2 CK Qbook 2008-2009).
48. D. Liver transplantation.
49. C. Asthma exacerbation.
50. B. Bronchoalveolar lavage (BAL) showed increased neutrophils.
51. E. Amiloride. Therapy in Liddle's syndrome consists of prescribing
amiloride or triamterene, potassium-sparing diuretics that directly block
the collecting tubule sodium channels and can correct both the
hypertension and, if present, the hypokalemia. The mineralocorticoid
antagonist spironolactone is ineffective since the increase in sodium
channel activity in Liddle's syndrome is not mediated by aldosterone..
52. E. Isotonic saline infusion.

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53. C. Severe Emphysema.
54. D. Hypopnea. No certain answer found.
55. B. Ciprofloxacin.
56. A. Restrictive changes by spirometry.
57. No certain answer found. B, D & E are all possible answers.
58. A. Enteral feeding at 72 hours is superior to TPN.
59. A. The patient will benefit from upper endoscopy.
60. D. Liver cirrhosis.
61. B. Liver biopsy.
62. E. No blood products.
63. A. Begin Allopurinol. Dose adjustment in renal disease – In patients
with stage 3 or greater chronic kidney disease (CKD; chronic renal
insufficiency), the starting dose of allopurinol and the rate of dose
adjustment should be modified. A daily starting dose of allopurinol of
<1.5 mg per mL/minute of estimated glomerular filtration rate (eGFR) is
advised in such patients, with dose increments of no more than 50 mg
daily every four weeks to the minimum daily dose necessary to achieve
the goal urate-lowering effect. As an example, for an eGFR of 50
mL/minute, the initial daily dose of allopurinol should not exceed 75 mg
daily. In patients with acute kidney injury (AKI; acute renal failure), it
may not be not advisable to initiate allopurinol, as the serum creatinine
during the acute episode will not initially reflect the severity of the
reduced renal function.
64. C. Caspfungin.
65. E. hemodialysis. Hemodialysis is indicated for this patient with
probable salicylate toxicity complicated by neurologic symptoms and
pulmonary edema. Salicylate toxicity causes mixed respiratory alkalosis
often with concurrent anion gap metabolic acidosis as noted in this
patient. Respiratory alkalosis usually predominates in adults with
salicylate toxicity, whereas anion gap metabolic acidosis is more
commonly the dominant acid-base disturbance in children. Hemodialysis
is indicated when serum salicylates levels exceed 100 mg/dl (7.2
mmol/L) or when there is persistent kidney dysfunction, fluid overload,
neurologic symptoms, pulmonary edema, or clinical deterioration despite
appropriate supportive care. When hemodialysis is not indicated,

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 intravenous sodium bicarbonate should be infused in patients with
salicylate toxicity. In patients requiring dialysis, intravenous sodium
bicarbonate should also be started pending initiation of hemodialysis
unless there is evidence of fluid overload or pulmonary edema as noted
in this patient. Increasing the arterial pH to 7.45- 7.6 facilitates
dissociation of H+ from the salicylate anion, creating a favorable
concentration gradient for H+-salicylate diffusion out of the central
nervous system. Intravenous sodium bicarbonate also promotes
increased salicylate clearance, with a goal to increase urine pH to >7.5
when possible. Patients with an alkalemic arterial pH should also receive
intravenous sodium bicarbonate to facilitate renal salicylate excretion,
and arterial blood gases should be closely monitored to keep the pH
<7.6. The addition of fomepizole to hemodialysis is not indicated. The
increased serum osmolality in this patient is primarily due to the
increased BUN, and the osmolar gap is only increased by 10 mOsm/kg,
making ethylene glycol and methanol unlikely. In addition, ethylene
glycol and methanol toxicity do not cause respiratory alkalosis. Although
acetazolamide alkalinizes the urine, its use is contraindicated in
salicylate toxicity because it lowers the arterial pH, thereby enhancing
the toxicity of salicylates. The differential diagnosis of mixed respiratory
alkalosis and anion gap metabolic acidosis includes salicylate toxicity,
sepsis, and acute liver failure. Salicylate toxicity is the most likely
diagnosis because the patient had a known suicide attempt with multiple
clinical features consistent with salicylate toxicity including fever,
mental status changes, mixed respiratory alkalosis and anion gap
metabolic acidosis, increased prothrombin time, thrombocytopenia, and
lactic acidosis. Broad-spectrum antibiotics are therefore not required for
this patient. Lithium toxicity may also require hemodialysis when
complicated by high lithium levels, depressed mentation, or seizures.
Lithium toxicity, however, does not cause severe acidosis. The patient's
lithium level is within the therapeutic range, essentially excluding
lithium as the cause of this patient's symptoms. Nausea, vomiting, and
diarrhea are common in lithium toxicity, often leading to hypovolemia
and decreased lithium clearance, and infusion of isotonic saline is often
required to correct hypovolemia. (Reference: MKSAP15).
Key Answers of Part 2 December 2019 - Nabeel Ibrahim Page 19
66. B. Imipenem and azithromycin.
67. C. Plasmapheresis. Polyarteritis nodosa (PAN) — In patients with
mild PAN, Guidelines suggest antiviral therapy alone. However, in
patients with PAN and severe manifestations (defined by the presence of
ulcerative or gangrenous lesions of the extremities, acute kidney injury
[AKI], polyneuropathy, central nervous system involvement, mesenteric
arteritis, or myocardial ischemia), Guidelines suggest both
glucocorticoids and plasmapheresis in addition to antiviral therapy
(preferably a nucleoside/nucleotide analog). The glucocorticoid and
plasmapheresis regimens that we use are as follows: Prednisone 0.7 to 1
mg/kg per day, tapered over four to six months; Plasma exchange, 2.5 to
4 liters per session for a total of 6 to 10 sessions, daily or on alternate
days, over two to three weeks. As with RPGN, antiviral therapy and
monitoring of HBV DNA levels are continued for at least six months
after cessation of immunosuppressive therapy or until the therapeutic
goal for hepatitis B is achieved, whichever is longer.
68. E. Around half of the patients requiring dialysis recover renal
function.
69. D. Pioglitazone. It is recognised that long term use of glitazone
therapy increases the risk of osteoporotic fracture. Data on both
pioglitazone and the now withdrawn rosiglitazone showed an increased
risk of fractures and animal models suggest this is due to reduced bone
mineral density. The underlying mechanism is thought to be due to bone
cell precursors differentiating into adipocytes rather than osteoblasts.
Data from the ADOPT study with rosiglitazone suggested that the rate of
fracture is intermediate between that of patients treated with a
sulphonylurea and a glitazone or metformin. Insulin and ramipril are not
known to be associated with increased risk of fracture. Thiazides such as
indapamide reduce calcium excretion and as such do not lead to
increased osteoporosis risk. (Reference: Reference: BMJ
OnExamination).
70. C. Mesothelioma.
71. E. Spontaneous pneumothorax.
72. A. 4.5 hours.

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73. C. Stage II. Chest x ray is abnormal in 85% of lung sarcoid, but 30-
60% are asymptomatic (that is, incidental chest x ray finding). Stage
Finding Likehood of spontaneous resolution
 0 Normal chest radiograph >90%
 I Bilat hilar lymphadenopathy (BHL) 60-90%
 II BHL plus pulmonary infiltrates 40-60%
 III Pulmonary infiltrates (no BHL) 10-20%
 IV Pulmonary fibrosis (+/- bullae) <20%
 (Reference: MRCP Part 1)
74. A. Barter’s syndrome.
75. C. Start IV duiretics.
76. E. Methylprednisolone. INITIAL THERAPY FOR PRIMARY
MCD: Choice of initial therapy — For most adults with primary minimal
change disease (MCD), Guidelines suggest initial therapy with
glucocorticoid monotherapy. For patients who cannot tolerate, have
contraindications to, or do not wish to take high-dose glucocorticoids,
glucocorticoid-sparing regimens are an alternative option and include
calcineurin inhibitors (CNI; cyclosporine or tacrolimus) or
mycophenolate mofetil/enteric-coated mycophenolate sodium
(MMF/EC-MPS) plus reduced-dose glucocorticoids. Dosing and
duration of these regimens are discussed elsewhere in this topic.
Glucocorticoid monotherapy leads to complete remission in 80 to over
95 percent of adults with MCD. The time course to a complete remission
is prolonged, with 50 percent responding by four weeks and 10 to 25
percent requiring more than three to four months of therapy. Most
glucocorticoid-responsive patients will respond by 16 weeks, but some
may respond as late as 21 weeks. In some adults, remission may be
observed during the period of tapering when a "fixed"-duration regimen
of glucocorticoids is used for induction of a remission. By contrast, most
children will respond within four weeks. (Reference: Mak SK, Short CD,
Mallick NP. Long-term outcome of adult-onset minimal-change
nephropathy. Nephrol Dial Transplant 1996; 11:2192.; Black DA, Rose
G, Brewer DB. Controlled trial of prednisone in adult patients with the
nephrotic syndrome. Br Med J 1970; 3:421.)
77. A. Hospital admission for intravenous labetalol.
Key Answers of Part 2 December 2019 - Nabeel Ibrahim Page 21
78. D. Clarithromycin. Clarithromycin: May increase the serum
concentration of Rivaroxaban. Risk C: Monitor therapy (UpToDate).
79. D. No antibiotics prophylaxis is required. Patients at highest risk —
Prophylaxis is suggested only in settings associated with the highest risk
of an adverse outcome if IE occurs. This includes patients with:
 Prosthetic heart valves, including mechanical, bioprosthetic, and
homograft valves (transcatheter-implanted as well as surgically
implanted valves are included)
 Prosthetic material used for cardiac valve repair, such as
annuloplasty rings and chords
 A prior history of IE
 Unrepaired cyanotic congenital heart disease
 Repaired congenital heart disease with residual shunts or
valvular regurgitation at the site or adjacent to the site of the
prosthetic patch or prosthetic device
 Repaired congenital heart defects with catheter-based
intervention involving an occlusion device or stent during the
first six months after the procedure
 Valve regurgitation due to a structurally abnormal valve in a
transplanted heart.
80. D. Metoprolol 12.5 mg BID.
81. D. Dual antiplatelet, iv nitrates and iv heparin.
82. B. Oral acyclovir.
83. E. Repeat Hep B serology. Non-responder. Test for current or
past infection. Give further vaccine course (i.e. 3 doses again) with
testing following. If still fails to respond then HBIG would be
required for protection if exposed to the virus.
84. E. DLCO.
85. A. Vancomycin + ceftriaxone. This patient most likely has bacterial
endocarditis and vertebral osteomyelitis. Since this patient is febrile and
ill appearing, it is appropriate to start empiric antibiotics as soon as
blood cultures have been drawn in order to pre- vent further
complications of infection. The most common pathogens in this type of
presentation are Staphylococcus aureus and the viridans Streptococci
(oral flora)—empiric treatment should be targeted toward treating these
Key Answers of Part 2 December 2019 - Nabeel Ibrahim Page 22
 organisms. Enterococci are a less frequent cause of endocarditis, though
still important to consider—empiric treatment for Staph and Strep will
also include empiric treatment for Enterococci. Coagulase-negative
Staphylococci are most common in patients with indwelling central
venous catheters, prosthetic heart valves, or other implanted cardiac
devices. Candidal endocarditis is most common among injection drug
users but still less common than the bacterial pathogens. Option A:
vancomycin provides empiric treatment for Staphylococcus aureus
(including MRSA) and the penicillin-resistant Enterococci, and
ceftriaxone provides empiric treatment for viridans Streptococci, so this
is the correct answer. Option B might be considered for prosthetic valve
endocarditis with MRSA, but this patient does not have a prosthetic
valve, rifampin is not indicated, and use of rifampin during active
bacteremia may lead to the development of rifampin resistance; hence,
this should not be used empirically or early in therapy. Option C:
nafcillin is excellent therapy for methicillin-susceptible Staphylococcus
aureus, but the possibility of MRSA has not been ruled out in this
patient, so he should receive vancomycin until cultures are documented,
and aminoglycosides (gentamicin) are no longer indicated for
Staphylococcus aureus bacteremia due to risk of nephrotoxicity and
minimal evidence of benefit. Option D: caspofungin (or micafungin,
both echinocandins) is excellent therapy for Candida infections, but
Candidal endocarditis is much less common than bacterial endocarditis,
even in injection drug users, so would not be chosen for empiric
treatment. Option E: ampicillin and gentamicin might be used for
treatment of penicillin-susceptible Enterococcal endocarditis, but it
would not be appropriate for empiric therapy in the absence of culture
data. (Reference: THE BRIGHAM INTENSIVE REVIEW OF
INTERNAL MEDICINE QUESTION AND ANSWER COMPANION).
86. B. Serum and urine protein electrophoresis. This patient presents
with nonspecific symptoms, anemia, and an elevated ESR. While these
symptoms might represent polymyalgia rheumatica (PMR), the
discrepantly low CRP warrants consideration of other processes. CRP is
a nonspecific indicator of inflammation that can be elevated because of
inflammation, infection, and some malignancies. In this case, factors
Key Answers of Part 2 December 2019 - Nabeel Ibrahim Page 23
 other than inflammation have led to an increased ESR; an
immunoglobulin paraproteinemia increases the ESR without affecting
the CRP because positively charged immunoglobulin promotes
electrostatic adhesion of negatively charged red blood cells such that
they settle out of suspension faster. In this case, the patient has multiple
myeloma, which would be detected by serum or urine electrophoresis
(SPEP/UPEP). There is nothing to suggest systemic lupus erythematosus
or other connective tissue disorder, so an antinuclear antibody is
unnecessary (Answer A). Temporal artery biopsy (Answer C) is used to
diagnose giant cell arteritis (GCA). Sometimes, GCA can present as
fever, malaise, and weight loss of unknown origin. CT scan imaging
(Answer D) can identify occult abscess or solid organ malignancy. Prior
to temporal artery biopsy or CT scan imaging, however, the discrepancy
in ESR and CRP first should be assessed with the much less invasive and
less costly SPEP/UPEP. Finally, it is inappropriate to treat the patient
empirically for PMR with low-dose corticosteroids (Answer E) until one
has ruled out other explanations for the patient’s complaints and
laboratory abnormalities. PMR should always be considered a diagnosis
of exclusion. (Reference: THE BRIGHAM INTENSIVE REVIEW OF
INTERNAL MEDICINE QUESTION AND ANSWER COMPANION).
87. D. Referral for surgical removal.
88. B. Phenylephrine. Phenylephrine: IV phenylephrine, an alpha1
agonist, is recommended for the treatment of acute hypotension in
obstructive HCM not responsive to fluid administration. In two case
series, phenylephrine (0.5 mcg/kg/min titrated to response) was useful in
patients who were acutely hypotensive owing to cardiogenic shock.
89. C. He can travel after 7 days from discharge.
90. B. Enrollment in a cardiac rehabilitation program is the most
important factor in returning to work after. In many hospitals, a
cardiac rehabilitation program with progressive exercise is initiated in
the hospital and continued after discharge. Ideally, such programs should
include an educational component that informs patients about their
disease and its risk factors. The usual duration of hospitalization for an
uncomplicated STEMI is about 3-5 days. The remainder of the
convalescent phase may be accomplished at home. During the first 1-2
Key Answers of Part 2 December 2019 - Nabeel Ibrahim Page 24
 weeks, the patient should be encouraged to increase activity by walking
about the house and out- doors in good weather. Normal sexual activity
may be resumed during this period. After 2 weeks, the physician must
regulate the patient's activity on the basis of exercise tolerance. Most
patients will be able to return to work within 2-4 weeks.
91. B. Mitral valve repair. In patients who have severe ischaemic mitral
regurgitation (grade 2 3/4 or, better, ERO > 20 mm2) and who should
undergo CABG, correction of mitral regurgitation should be undertaken.
Valve repair is frequently preferred, provided the surgeons have
expertise with this technique and a careful intraoperative evaluation can
be performed with the knowledge of potential pitfalls regarding
quantification. When the type of coronary revascularisation is debated,
the association of severe ischaemic mitral regurgitation leads to
combined surgery rather than percutaneous intervention.
(https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1769268/?fbclid=IwA
R0iVHZ4qa-3W1dOppcUcv87Wdhn0uc3PIb-
2DqOXdRt92T_uQXahEwNiGg)
92. B. Her temperature may have exacerbated her ECG changes.
Fever can be a trigger for both induction of Brugada pattern ECG
abnormalities and cardiac arrest among persons known to have Brugada
pattern ECG or Brugada syndrome. Animal models have helped
elucidate how hyperthermia causes changes in sodium current function.
A reduction in sodium current results in changes to the action potential
predisposing to VF. (Morita H, Zipes DP, Morita ST, Wu J. Temperature
modulation of ventricular arrhythmogenicity in a canine tissue model of
Brugada syndrome. Heart Rhythm 2007; 4:188.)
93. E. Induce sputum with staining for Pneumocystis.
94. B. Aspirin plus low molecular weight heparin. The evidence base
to make an informed choice is not particularly strong. Aspirin plus
unfractionated heparin has been found to be associated with a better fetal
outcome than aspirin alone (80% versus 40% live birth rate) and two
small trials have suggested that aspirin plus low molecular weight
heparin is equivalent to aspirin plus unfractionated heparin. Use of
unfractionated heparin in pregnancy is generally avoided because of the
risk of osteoporosis and haemorrhage. The British Committee for

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 Standards in Haematology (BCSH) advice for a patient such as the one
described is that aspirin plus low molecular weight heparin be given.
(Reference: Multiple Choice Questions for Haematology and Core
Medical Trainees).
95. D. Heterozygosity for either B thalassaemia or haemoglobin S.
The diagnosis in the young woman is haemoglobin S/B+ thalassaemia
compound heterozygosity. Of relevance in her partner would be B
thalassaemia heterozygosity (with a risk of either B thalassaemia major
or haemoglobin S/B thalassaemia compound heterozygosity in the fetus)
or haemoglobin S (risk of sickle cell anaemia or haemoglobin S/B
thalassae-mia compound heterozygosity in the fetus). There is no reason
to suspect an underlying a thalassaemia so neither aº thalassaemia
heterozygosity nor haemoglobin H disease would be relevant. Note that
both haemoglobin S and B thalassaemia occur in Sicily. B thalassaemia
is highly prevalent and haemoglobin S heterozygosity occurs in about
2% of Sicilians. (Reference: Multiple Choice Questions for
Haematology and Core Medical Trainees).
96. E. Anti-HMGCR.
97. D. Give blood transfusion, admit to hospital and ensure adequate
hydration.
98. B. 70/80. PPV = TP / (TP+FP), TP is 70 (positive test and confirmed
by echocardiography), and FP is 10 (positive test that did not confirmed
by echocardiography).
99. C. Efficacy.
100. D. The trachea divides into right and left main stem bronchi
below the sterna angle. At the carina, the trachea splits into the right
and left main bronchi. As a reference point, the carina lies approximately
in line with the sternal angle, which is the junction of the manubrium and
body of the sternum (angle of Louis). (Respiratory Care: Patient
Assessment and Care Plan Development David C. Shelledy Jay I. Peter)
101. C. Fluconazole.
102. D. Wilson's disease.
103. D. Pneumocystis jirovecii.
104. D. Discoid Lupus.
105. A. Stellate ganglion block. Stellate ganglion block causes
sympathetic blockade of the ipsilateral face and arm. Therefore, a

Key Answers of Part 2 December 2019 - Nabeel Ibrahim Page 26

 successful block produces an ipsilateral Horner's syndrome (ptosis,
miosis, and anhydrosis), flushing of the face, and increased temperature
of the arm. These effects are normal and last for the duration of the
blockade.
106. C. Subdural hematoma.
107. D. Kaposi's sarcoma.
108. A. Pseudogout. Cartilage calcification (chondrocalcinosis) —
Radiographic evidence of CPPD is the defining feature of this finding.
CPPD typically appears as punctate and linear radiodensities in articular
cartilage (fibrocartilage and/or hyaline cartilage) and, with lesser
frequency, in ligaments, tendons, synovia, bursae, and joint capsules.
Although deposits of basic calcium phosphate crystals may occasionally
cause confusion, such deposits are usually faint and are irregularly
contoured.
109. A. Dermatitis herpetiformis.
110. A. Acute promyelocytic leukemia. Coagulopathy and APL —
Coagulopathy associated with APL is complex and involves both
disseminated intravascular coagulation (DIC) and primary
hyperfibrinolysis and is either present at diagnosis or occurs soon after
the initiation of cytotoxic chemotherapy. This complication constitutes a
medical emergency, because, if left untreated, it can cause pulmonary or
cerebrovascular hemorrhage in up to 40 percent of patients and a 10 to
20 percent incidence of early hemorrhagic death. Thrombotic
complications are less common.

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TOP REFERENCES:
1. Harrison's Principles of Internal Medicine Self-Assessment and
Board Review, 19th Edition.
2. OnExamination Part 1.
3. Kaplan USMLE Step 2 CK Qbook 2008-2009.
4. European Respiratory Society | Self-Assessment in Respiratory
Medicine.
5. Course - Neurology 4th edition.
6. Kaplan Internal Medicine Question Book.
7. PreTest Medicine 14e
8. MKSAP18.
9. THE BRIGHAM INTENSIVE REVIEW OF INTERNAL MEDICINE
QUESTION AND ANSWER COMPANION.
10. Lange Q & A INTERNAL MEDICINE 5e.
11. Multiple Choice Questions for Haematology and Core Medical
Trainees.

Key Answers of Part 2 December 2019 - Nabeel Ibrahim Page 28

Note: Please write for me, if you find a certain answer or reference.
 Email: [email protected]
 Telegram: +9647703033141

Nabeel Ibrahim Khaleel

M.B.Ch.B. [Mosul College of Medicine]

SHO in Internal Medicine [Arab Board]

Baghdad Teaching Hospital

December 2021

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