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Budd-Chiari syndrome is caused by the obstruction of the

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A key risk factor for Budd-Chiari syndrome, which presents
with jaundice, ascites, and hepatomegaly, is
{{c1::polycythemia vera}}.

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Budd-Chiari syndrome often presents with elevated liver
enzymes, jaundice, and abdominal pain localized to the
{{c1::right upper}} quadrant.

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Hereditary hemochromatosis is characterized by excessive
absorption and deposition of {{c1::iron}} in various organs.

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The diagnosis of hereditary hemochromatosis includes
elevated serum {{c1::ferritin}} and transferrin saturation
levels.

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Hereditary hemochromatosis is an {{c1::autosomal
recessive}} disorder.

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Polycythemia vera is characterized by an increased {{c1::red
blood cell}} mass.
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Diagnosis of polycythemia vera is confirmed by elevated
hemoglobin/hematocrit and low {{c1::erythropoietin}} levels.

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A common mutation found in polycythemia vera is the
{{c1::JAK2}} mutation.
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Chediak-Higashi Syndrome is an autosomal recessive disorder
caused by mutations in the {{c1::LYST}} gene.
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A characteristic feature of Chediak-Higashi Syndrome is the
presence of {{c1::giant granules}} in neutrophils and other
leukocytes.
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Physical findings in Chediak-Higashi Syndrome include
partial {{c1::albinism}} and recurrent {{c1::infections}} due
to impaired neutrophil function.
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Exogenous T3 supplementation {{c1::suppresses::action}}
TSH levels by increasing negative feedback, which in turn
decreases T4 secretion from the thyroid gland. Furthermore,
reverse T3 (rT3) {{c1::decreases::effect on rT3}} because less
T4 is available for conversion.
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TSH from the anterior pituitary stimulates the thyroid to
produce thyroxine (T4) and a small amount of triiodothyronine
(T3). T4 is converted in peripheral tissues to {{c1::T3 (active
form)}} and {{c1:: reverse T3 (inactive form)}}.
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Iron bound to heme is normally in the reduced ferrous
({{c1::Fe2+::state of iron in heme normally}}) state. Nitrites
cause poisoning by inducing the conversion of this heme iron
to the oxidized ferric ({{c1::Fe3+::oxidized state}}) state,
leading to the formation of ({{c1::methemoglobin}}.
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Front: Methemoglobinemia causes {{c1::dusky::type of
discoloration}} discoloration of the skin (similar to cyanosis),
and because methemoglobin is unable to carry oxygen, a state
of functional anemia is induced.
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Anaphylaxis is a systemic type I hypersensitivity reaction
characterized by increased vascular permeability and
multisystem edema, leading to massive shifting of
intravascular fluid to the extravascular compartment.
Symptoms often begin within {{c1::seconds to
minutes::timeline}} after intravascular exposure to an inciting
factor (e.g., insect stings, intravenous medications) but can
take up to 2 hours to develop with orally ingested antigens.
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Anaphylaxis results from widespread {{c1::mast cell and
basophil degranulation::cells involved}} and resultant
{{c1::histamine and tryptase::substances released}} release.
The latter, is an enzyme that is relatively specific to mast cells,
and elevated serum levels of it are often used to support a
clinical diagnosis of anaphylaxis after the patient has been
stabilized.
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The high-affinity IgE receptor (FcεRI) is found on the surface
of mast cells and basophils and normally binds the Fc portion
of circulating IgE antibodies. Cross-linking of multiple
membrane-bound IgE antibodies by a multivalent antigen
results in {{c1::aggregation of the FcεRI
receptors::mechanism triggered by multivalent antigen}}.

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Front: {{c1::Aggregation::process}} of the FcεRI receptors on
mast cells and basophils causes degranulation and the release
of preformed mediators (e.g., histamine, tryptase) that initiate
an allergic response.

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Front: A 57-year-old man with a history of type 2 diabetes,
obesity, hyperlipidemia, hypertension, and gout presents with
nausea, vomiting, and severe crampy pain in the right flank.
Abdominal ultrasound reveals right-sided hydronephrosis and
proximal ureteral dilation. Urinalysis would most likely reveal
the presence of {{c1::red blood cells (RBCs)::substance}} in
the urine.

Card #22
Front: In ureterolithiasis, the disruption of the ureteral
epithelium typically results in hematuria with
{{c1::normal::RBC morphology in ureterolithiasis}}
morphology of RBCs, differentiating it from glomerular
causes of hematuria where {{c1::RBC casts::RBC morphology
in glomerular causes}} are found in the urine.

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Front: A 15-year-old boy presents with right arm numbness,
fluctuating tingling, and numbness involving the right
shoulder, arm, and hand. The symptoms worsen with overhead
activities and throwing a baseball. This condition is most
likely due to compression of the brachial plexus within the
{{c1::scalene triangle::location}}, bordered by the anterior and
middle scalene muscles and the first rib.

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Front: In thoracic outlet syndrome (TOS), compression of the
brachial plexus occurs as it passes through the scalene triangle,
which is formed by the {{c1::anterior and middle
scalene::muscles}} muscles and the first rib. Patients often
present with upper extremity numbness, tingling, and
weakness.

Card #25
Front: A 43-year-old immigrant from Southern Asia with a
history of cough and recent hemoptysis, reports 15-lb weight
loss over the past four months. Sputum cultures grow acid-fast
bacilli that are susceptible to most antimycobacterial drugs in
vitro. Isoniazid monotherapy in this patient would most likely
result in {{c1::selective survival of bacterial cells secondary to
gene mutation::outcome}}.

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Front: Isoniazid resistance in Mycobacterium tuberculosis
specifically occurs due to two selective gene mutations. The
first is a decrease in bacterial expression of the {{c1::catalase-
peroxidase::enzyme}} enzyme required for isoniazid
activation, and the second is through modification of the
{{c1::protein target::binding site}} binding site.

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Front: Celiac disease is a chronic malabsorptive disorder
caused by a hypersensitivity to {{c1::gluten::protein}}, a
protein found in wheat, barley, and rye. This triggers an
immune-mediated reaction causing {{c1::villous
atrophy::immune reaction effect}}, {{c1::crypt
hyperplasia::effect}}, and intraepithelial lymphocyte
infiltration.

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Front: Screening for celiac disease is done with serology
testing for elevated IgA {{c1::anti-endomysial::antibody}}
and anti-tissue {{c1::transglutaminase::antibody}} antibodies.
Diagnosis is confirmed by {{c1::endoscopic
biopsy::diagnostic method}}, and treatment involves a
{{c1::gluten-free::diet}} diet.

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Front: Acetylcholinesterase inhibitors improve skeletal muscle
weakness (Ach, nicotinic) but can cause {{c1::muscarinic
overstimulation::effect}} of the smooth muscles and excessive
glandular secretions (e.g., diarrhea, diaphoresis, abdominal
cramping, emesis). Selective {{c1::muscarinic
antagonists::medications}} (e.g., glycopyrrolate, hyoscyamine,
propantheline) can be used to reduce these adverse effects
without affecting the action of cholinesterase inhibitors on
skeletal muscle.
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Front: Drug-induced lupus erythematosus (DILE) should be
considered in patients presenting with signs and symptoms of
systemic lupus erythematosus (SLE). Both
{{c1::hydralazine::drug 1}} and {{c1::procainamide::drug 2}}
are categorized as high-risk drugs for the development of
DILE. Other implicated drugs include isoniazid, minocycline,
and quinidine.

Card #31
Front: ST-segment elevation in the inferior leads is diagnostic
of an inferior myocardial infarction (MI). Inferior MIs are
often due to blockage of the {{c1::right coronary
artery::artery}}, the artery usually responsible for sinoatrial
(SA) and atrioventricular (AV) node perfusion. Thus, inferior
MIs are often associated with bradycardia.

Card #32
Front: Atropine blocks vagal influence on the SA and AV
nodes and is effective in increasing heart rate in patients with
bradycardia. However, in the eye, atropine causes
{{c1::mydriasis::effect on eye}}, resulting in narrowing of the
anterior chamber angle and diminished outflow of aqueous
humor. This can precipitate {{c1::angle-closure
glaucoma::condition}} in patients with shallow anterior
chambers or higher than normal intraocular pressures.
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Front: A hypertensive emergency is defined by a systolic
blood pressure ≥180 mm Hg or diastolic pressure ≥120 mm
Hg along with evidence of {{c1::end-organ
damage::condition}}.

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Front: Labetalol is a nonselective vasodilatory beta blocker
that blocks beta-1, beta-2, and alpha-1 adrenergic receptors.
The alpha-1 receptor blockade outweighs beta-2 receptor
blockade in vascular smooth muscle to cause {{c1::peripheral
vasodilation::effect}}, leading to decreased {{c1::systemic
vascular resistance::outcome}} and heart rate.

Card #35
Front: A major polysaccharide component of the fungal cell
wall is {{c1::1,3-beta-D-glucan::polysaccharide}}.
Caspofungin and the other echinocandin antifungals (e.g.,
micafungin) block {{c1::glucan::synthesis}} synthesis.

Card #36
Front: Caspofungin is most active against
{{c1::Candida::fungus 1}} species and
{{c1::Aspergillus::fungus 2}}. It is not active against
{{c1::Cryptococcus neoformans::fungus 3}} and has limited
activity against Mucor and Rhizopus species.

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Front: Coronary sinus dilation seen on echocardiography is
usually an indication of elevated {{c1::right-sided heart
pressure::pressure}}, as occurs with {{c1::pulmonary
hypertension::condition}}.

Card #38
Front: HIV enters the central nervous system via infected
monocytes and establishes a productive infection in
{{c1::microglial cells::CNS macrophages}} (resident
macrophages of the central nervous system) and blood-derived
perivascular macrophages. Activation of these cells leads to
the formation of {{c1::microglial nodules::structure 1}} and
{{c1::multinucleated giant cells::structure 2}}.