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* NBME 4 answer key?????
  abababab - 09/08/10 18:01
  Can anybody please share the answer key to NBME 4

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* Re:NBME 4 answer key?????
  shanma - 09/08/10 18:30
  The following is from an old post. Explanations for block 1 only.
Sorry, I don't have the whole set.

let's everyone will contribute detailed explanation for some NBME question.
so we finally will have detailed answers for whole NBME..
here is my contribution...

Form 4-1

Zinc finger motif is a DNA binding domain for steroid receptor.
Zinc fingers are small protein structural motifs that can coordinate one or more zinc ions to help stabilize
their folds. They can be classified into several different structural families and typically function as
interaction modules that bind DNA, RNA, proteins or small molecules.

Glycogen storage disease type V (GSD-V) is a metabolic disorder, more specifically a glycogen storage disease,
caused by a deficiency of myophosphorylase.[1] It is the most common of the various types of glycogen storage
disease, but is still considered rare (1 in 100,000).

GSD type V is also known as McArdle's disease or muscle phosphorylase (myophosphorylase) deficiency. The disease
was first reported in 1951 by Dr. Brian McArdle of Guy's Hospital, London.[2]
The onset of this disease is usually noticed in childhood,[3] but often not diagnosed until the third or fourth
decade of life. Symptoms include exercise intolerance with myalgia, early fatigue, painful cramps, weakness of
exercising muscles and myoglobinuria. Myoglobinuria, the condition where myoglobin is present in urine, may
result from serious damage to the muscles, or rhabdomyolysis, where muscle cells breakdown, sending their
contents into the bloodstream.
The deficiency was the first metabolic myopathy to be recognized, when Dr. McArdle described the first case in
a 30-year-old man who always experienced pain and weakness after exercise. Dr. McArdle noticed this patient’s
cramps were electrically silent and his venous lactate levels failed to increase upon ischemic exercise.
(The ischemic exercise consists of the patient squeezing a hand dynamometer at maximal strength for a specific
period of time, usually a minute, with a blood pressure cuff, which is placed on the upper arm and set at
250 mmHg, blocking blood flow to the exercising arm.) Notably, this is the same phenomenon that occurs when
muscle is poisoned by iodoacetate, a substance that blocks breakdown of glycogen into glucose and prevents the
formation of lactic acid. Dr. McArdle accurately concluded that the patient had a disorder of glycogen breakdown
that specifically affected skeletal muscle. The associated enzyme deficiency was discovered
in 1959 by W. F. H. M. Mommaerts et al.

Patients may exhibit a “second wind” phenomenon. This is characterized by the patient’s ability, after resting,
to resume their normal activities. This is attributed to the combination of increased blood flow and the ability
of the body to find alternative sources of energy, like fatty acids and proteins. In the long term, patients may
exhibit renal failure due to the myoglobinuria, and with age, patients may exhibit progressively increasing
weakness and substantial muscle loss.

Epidermolysis bullosa simplex (EBS) is a disorder resulting from mutations in the genes encoding keratin 5 or
keratin 14.[1]:598

Blister formation of EBS is within the basal keratinocyte of the epidermis. Sometimes EBS is called epidermolytic
Epidermolysis bullosa (EB) is a rare genetic disorder caused by a mutation in the keratin gene. The disorder is
characterized by the presence of extremely fragile skin and recurrent blister formation, resulting from minor
mechanical friction or trauma. The condition was brought to public attention in the UK through the Channel 4
documentary The Boy Whose Skin Fell Off, chronicling the life and death of Jonny Kennedy, an English man with EB.
The skin has two layers; the outer layer is called the epidermis and the inner layer the dermis. In normal
individuals, there are "anchors" between the two layers that prevent them from moving independently from one
another. In people born with EB, the two skin layers lack the anchors that hold them together, and any action
that creates friction between the layers (like rubbing or pressure) will create blisters and painful sores.
Sufferers of EB have compared the sores to third-degree burns.[2]

"Butterfly Children" is a term often used to describe younger patients because the skin is said to be as fragile
as a butterfly’s wings.[3]

Children with the condition have also been described as "Cotton Wool Babies," [4][5] and in South America,
"Crystal Skin Children" is the term used. [6]

Tight junctions, or zonula occludens, are the closely associated areas of two cells whose membranes join together
forming a virtually impermeable barrier to fluid.

CF is autosomal recessive disease ... the child with diease is homozygous
for CF gene.. carrier are heterogygous for the mutation...
For the parent to produce a homozygous child they must both be carrier of the
Only if both parents are carrier (or one carrier, another diseased) their children could be diseased (homozygous)
In this case both parents carriers (there is no information in question stem assuming one is diseases)
So if both parents are heterozygous (Aa)
1/4 would be (AA) homozygous normal
2/4 would be (Aa) heterozygous carrier
1/4 would be (aa) homozygous diseased

As question asks likelihood that of unaffeted child being a carrier
2/3 the answer. this child is unaffected, and he could be only normal or carrier.

a. could be but never heard
c. homeobox genes are active only during early embryonal morphogenesis. there no need to activate them again in
d. An oncogene is a gene that, when mutated or expressed at high levels, helps turn a normal cell into a
tumor cell.
so only B make sense (f.e. Adenine deaminase gene treatment for SCID)

a.adenocarcinoma has a glandular appearance.
b. malignant melanoma. A diagnosis of melanoma is supported by the presence of the S-100 protein marker.
c. non-Hodgkin lymphoma = CD45
d. sarcoma = vimentin
e.squamous cell carcinoma the tumor cell ar similar to normal squamous epithelial cells, with intercellular bridges
and nest of keratin pearls.

8-B collect more information

increased serum ketone bodies could be due to fatty acid catobolism. But blood urea nitrogen produced only from
amino acids. During starvation skeletal muscle protein used for gluconeogenesis. as bypruduct of it is increased
urea production
a. there is no much protein in wild berries
b. hepatic glycogen stores are depleted after 10-18 hours.
c. skeletal muscle glycogen is used only for muscle's own needs. muscles does not have glucose 6 phosphatase, so
skeletal muscle can't secrete free glucose into the blood.
e. urea is a waste product, not a substrat for gluconeogenesis.
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* Re:let's make database of NBME answers
goforward - 01/28/10 11:32

d. Quinidine
Like all other class I antiarrhythmic agents, quinidine primarily works by blocking the fast inward sodium
current (INa). Quinidine's effect on INa is known as a use dependent block. This means that at higher heart rates,
the block increases, while at lower heart rates the block decreases. The effect of blocking the fast inward
sodium current causes the phase 0 depolarization of the cardiac action potential to decrease (decreased Vmax).
Quinidine is also an inhibitor and an inducer of the cytochrome P450 enzyme 2D6, and can lead to increased blood levels of lidocaine, Beta blockers, opioids, and some anti-depressants.

Quinidine also inhibits the transport protein P-glycoprotein and so can cause some peripherally acting drugs such
as loperamide to have CNS side effects such as respiratory depression if the two drugs are co-administered.[1]

Quinidine-induced thrombocytopenia (low platelet count) is mediated by the immune system, and may lead to
thrombocytic purpura. Discovered by a Danish Merchant seaman with AF who took quinine for malaria prophylaxis
during trips to India. He noted his pulse was regular while in India but irregular at home. Chichonism describes
tinnitus and hearing loss with quinidine excess.

Quinidine can cause thrombocytopenia, granulomatous hepatitis, myasthenia gravis, and torsades de pointes and for
that reason is not used much today. Torsades can occur after the first dose.

Quinidine intoxication can lead to a collection of symptoms collectively known as cinchonism with tinnitus
(ringing in the ears) being among the most characteristic and common symptoms of this toxicity syndrome.

Properly speaking, benzopyrene is a procarcinogen, meaning that the mechanism of carcinogensis of benzopyrene depends on enzymatic metabolism of benzopyrene to the ultimate mutagen, benzopyrene diol epoxide. This molecule intercalates in DNA, covalently bonding to the nucleophilic guanine nucleobases at the N2 position. X-ray crystallographic and nuclear magnetic resonance structure studies show that this binding distorts the DNA,[10] inducing mutations by perturbing the double-helical DNA structure. This disrupts the normal process of copying DNA and induces mutations, which explains the occurrence of cancer after exposure. This mechanism of action is similar to that of aflatoxin which binds to the N7 position of guanine.[11]

There are indications that benzopyrene diol epoxide specifically targets the protective p53 gene.[12] This gene is a transcription factor that regulates the cell cycle and hence functions as a tumor suppressor. By inducing G (guanine) to T (thymidine) transversions in transversion hotspots within p53, there is a probability that benzopyrene diol epoxide inactivates the tumor suppression ability in certain cells, leading to cancer.

Benzopyrene diol epoxide is the carcinogenic product of three enzymatic reactions:

1. Benzopyrene is first oxidized by cytochrome P4501A1 to form a variety of products, including (+)benzopyrene 7,8 epoxide.[13]
2. This product is metabolized by epoxide hydrolase, opening up the epoxide ring to yield
(-)benzo[a]pyrene 7,8,dihydrodiol.
3. The ultimate carcinogen is formed after another reaction with cytochrome P4501A1 to yield the (+)benzopyrene -7,8 dihydrodiol-9,10 epoxide. It is this diol epoxide that covalently binds to DNA.

NBME 4_1
The most serious complication of bleomycin is pulmonary fibrosis and impaired lung function.
in pulmonary fibrosis (restrictive lung disease) lung compliance will decrease, therefore total lung volume will also decrease. Due to increase of the thickness of alveolo-arteriolar septum diffusing capacity of oxygen and carbon dioxide will decrease. FEV and FVC will decrease, so FVC/FVC ratio will no change or increase.

4.1.17. The Question asks us the how many women need to be treated to prevent one vertebral fracture or NNT.
NNT = 1/Absolute risk reduction
ARR = Event rate(control) - Event rate(treated)
event rate for control=260/2576=10.1%
event rate for treated=138/2557=5.4%
NNT = 1/4.7%
NNT = 100/4.7 = 21.2

Vibrio parahaemolyticus is a curved, rod-shaped, Gram-negative bacterium found in brackish [1] saltwater, which,
when ingested, causes gastrointestinal illness in humans.[1] V. parahaemolyticus is oxidase positive,
facultatively aerobic, and does not form spores. Like other members of the genus Vibrio, this species
is motile, with a single, polar flagellum.[2]

While infection can occur via the fecal-oral route, ingestion of bacteria in raw or undercooked seafood,
usually oysters, is the predominant cause the acute gastroenteritis caused by V. parahaemolyticus.[3] Wound
infections also occur, but are less common than seafood-borne disease. The disease mechanism of V. parahaemolyticus
infections has not been fully elucidated.[4] However, most clinical disease results from strains that carry
either the thermostable direct hemolysin gene (tdh) or the tdh-related hemolysin gene (trh) or both genes.
Outbreaks tend to be concentrated along coastal regions during the summer and early fall when higher water
temperatures favor higher levels of bacteria. Seafood most often implicated includes squid, mackerel, tuna,
sardines, crab, shrimp, and bivalves like oysters and clams. The incubation period of ~24 hours is followed by
explosive, watery diarrhea accompanied by nausea, vomiting, abdominal cramps, and sometimes fever.
Vibrio parahaemolyticus symptoms typically resolve with-in 72 hours, but can persist for up to 10 days
in immunocompromised individuals. As the vast majority of cases of V. parahaemolyticus food infection are
self-limiting, treatment is not typically necessary. In severe cases, fluid and electrolyte replacement is

Additionally, swimming or working in affected areas can lead to infections of the eyes or ears [5] and open
cuts and wounds. Following Hurricane Katrina, there were 22 vibrio wound infections 3 of which were caused by
V. parahaemolyticus and 2 of these led to death.

38. C.
Cystic fibrosis (also known as CF or mucoviscidosis) is a common hereditary disease which affects the entire body,
causing progressive disability and often, early death. The name cystic fibrosis refers to the characteristic
scarring (fibrosis) and cyst hairy within the pancreas, first recognized in the 1930s.[1] Difficulty breathing
is the most serious symptom and results from frequent lung infections that are treated, though not cured, by
antibiotics and other medications. A multitude of other symptoms, including sinus infections, poor growth,
diarrhea, and infertility result from the effects of CF on other parts of the body.

CF is caused by a mutation in a gene called the cystic fibrosis transmembrane conductance regulator (CFTR).
This gene helps create sweat, digestive juices, and mucus. Although most people without CF have two working copies
of the CFTR gene, only one is needed to prevent cystic fibrosis. CF develops when neither gene works normally.
Therefore, CF is considered an autosomal recessive disease.

CF is most common among Caucasians and Ashkenazi Jews; one in 25 people of European descent carry one gene for CF.
Approximately 30,000 Americans have CF, making it one of the most common life-shortening inherited diseases.
Individuals with cystic fibrosis can be diagnosed prior to birth by genetic testing or in early childhood by
a sweat test. There is no cure for CF, and most individuals with cystic fibrosis die young — many in their 20s
and 30s from lung failure. Ultimately, lung transplantation is often necessary as CF worsens.
The hallmarks of cystic fibrosis are salty tasting skin, normal appetite but poor growth and poor weight gain,
excess mucus production, frequent chest infections and coughing/shortness of breath. Males can be infertile
due to congenital absence of the vas deferens. CF symptoms often appear in infancy and childhood, with meconium
ileus being a typical finding in newborn babies. As the child grows, he or she will have to exercise to release
mucus stuck to the alveoli. Cilial epithilial cells in the patient have a mutated protein that instead of
creating the right resin that is used to prevent the alveoli from collapsing, it makes a thicker resin, mucus.
Poor growth is a hallmark of CF. Children with CF typically do not gain weight or height at the same rate as
their peers, and occasionally are not diagnosed until investigation is initiated for poor growth. The causes
of growth failure are multi–factorial and include chronic lung infection, poor absorption of nutrients through
the gastrointestinal tract, and increased metabolic demand due to chronic illness.

Cimetidine (INN) (pronounced /s??m?t?di?n/, /sa??m?t?di?n/) is a histamine H2-receptor antagonist that inhibits the
production of acid in the stomach. It is largely used in the treatment of heartburn and peptic ulcers. It is
marketed by GlaxoSmithKline under the trade name Tagamet (sometimes Tagamet HB or Tagamet HB200) and was approved
in the US by the Food & Drug Administration for prescriptions starting January 1, 1979.

Glomerular filtration rate
GFR = Kf [(PGC - PBS) - (oGC - oBS)]
GFR = 3 x [(45-12) - (23-0)] = 3 x [33 - 23] = 3 x 10 = 30

Renal cell carcinoma
Compare with Goljian slide. Renal 42.
This slide demonstrates the microscopic findings of
a renal cell carcinoma. The tumor cells derived
from the proximal tubule are clear and vacuolated
in appearance.

This patient probably has left renal artery atherosclerosis, which leads to decresed blood flow in left kidney. In
response kidney increase renin secretion. Which leads to increase angiotensin 2, and subsequently aldosterone will
also increase.

Letdown reflex – in lactating (breastfeeding) mothers, oxytocin acts at the mammary glands, causing milk to be
'let down' into a collecting chamber, from where it can be extracted by compressing the areola and sucking at the
nipple. Sucking by the infant at the nipple is relayed by spinal nerves to the hypothalamus. The stimulation
causes neurons that make oxytocin to fire action potentials in intermittent bursts; these bursts result in the
secretion of pulses of oxytocin from the neurosecretory nerve terminals of the pituitary gland.

44. C
Polycystic ovary syndrome (PCOS) is one of the most common female endocrine disorders affecting approximately
5%-10% of women of reproductive age (12-45years old) and is one of the leading causes of infertility.
The principal features are obesity, anovulation (resulting in irregular menstruation), acne, and excessive amounts
or effects of androgenic (masculinizing) hormones. The symptoms and severity of the syndrome vary greatly among
women. While the causes are unknown, insulin resistance, diabetes, and obesity are all strongly correlated with
Common symptoms of PCOS include

Oligomenorrhea, amenorrhea — irregular, few, or absent menstrual periods.
Infertility, generally resulting from chronic anovulation (lack of ovulation).
Hirsutism — excessive and increased body hair, typically in a male pattern affecting face, chest and legs.
Hair loss appearing as thinning hair on the top of the head
Acne vulgaris, seborrhoeic dermatitis.
Obesity or weight gain: one in two women with PCOS are obese[citation needed].
Deepening of voice
Mild symptoms of hyperandrogenism, such as acne or hyperseborrhea, are frequent in adolescent girls and are
often associated with irregular menstrual cycles. In most instances, these symptoms are transient and only
reflect the immaturity of the hypothalamic-pituitary-ovarian axis during the first years following menarche.[9]

PCOS can present in any age during the reproductive years. Due to its often vague presentation it can take years
to reach a diagnosis.
PCOS clue is decreased FSH

45-B Ductus venosus runs through the liver
In the fetus, the ductus venosus shunts a significant majority (80%) of the blood flow of the umbilical vein
directly to the inferior vena cava. Thus, it allows oxygenated blood from the placenta to bypass the liver.
In conjunction with the other fetal shunts, the foramen ovale and ductus arteriosus, it plays a critical role
in preferentially shunting oxygenated blood to the fetal brain.

The ductus venosus is open at the time of the birth and is the reason why umbilical vein catheterization works.
Ductus venosus naturally closes during the first week of life in most full-term neonates; however, it may take
much longer to close in pre-term neonates. Functional closure occurs within minutes of birth. Structural closure
in term babies occurs within 3 to 7 days.

After it closes, the remnant is known as ligamentum venosum.

If the ductus venosus fails to occlude after birth, the individual is said to have an intrahepatic
portosystemic shunt (PSS). This condition is hereditary in some dog breeds (e.g. Irish Wolfhound).

Regulation of PTH secretion
Secretion of parathyroid hormone is chiefly controlled by serum [Ca2+] through negative feedback, which
is achieved by the activation of calcium-sensing receptors located on parathyroid cells.[9] Calcium sensing
receptors work by activating the phospholipase C pathway,[10][11] presumably through a Gq? type of G protein,
which ultimately increases intracellular concentration of calcium, which triggers vesicle fusion and exocytosis
of parathyroid hormone. It also inhibits (not stimulates, as some[12] sources state) the cAMP dependent pathway.

Decreased serum [Ca2+].
Mild decreases in serum [Mg2+].
An increase in serum phosphate (Since increased phosphate will complex with serum calcium to form calcium
phosphate, this causes the Ca sensitive receptors (CaSr) to think that serum Ca has decreased, as CaSR do not
sense Calcium phosphate, thereby triggering an increase in PTH)

Increased serum [Ca2+].
Severe decreases in serum [Mg2+], which also produces symptoms of hypoparathyroidism (such as hypocalcemia).

Papillary adenocarcinoma
Most common primary cancer in adults and children
Female dominant
Associated with radiation exposure
Papillary thyroid cancer is the most common type of thyroid cancer.[1] It occurs more frequently in women and
presents in the 30-40 year age group. It is also the predominant cancer type in children with thyroid cancer,
and in patients with thyroid cancer who have had previous radiation to the head and neck.

48-E Octreotide a long acting somatostatin
The Food and Drug Administration (FDA) has approved the usage of a salt form of this peptide, octreotide acetate,
as an injectable depot formulation for the treatment of acromegaly, the treatment of diarrhea and flushing
episodes associated with carcinoid syndrome, and treatment of diarrhea in patients with vasoactive intestinal
peptide-secreting tumors (VIPomas).

Octreotide has also been used off-label for the treatment of severe, refractory diarrhea from other causes. It is
used in toxicology for the treatment of prolonged recurrent hypoglycemia after sulfonylurea and possibly
meglitinides overdose.

Octreotide has also been used with varying degrees of success in infants with nesidioblastosis to help decrease
insulin hypersecretion.

In patients with suspected esophageal varices, octreotide can be given to help decrease bleeding.[3]

Octreotide has been investigated for patients with pain from chronic pancreatitis.[4]

Octreotide may be useful in the treatment of thymic neoplasms.

Octreotide has been used as an unlicensed drug, injected sub-cutaneously in the management of hypertrophic
pulmonary osteoarthropathy (HPOA), secondary to non-small cell lung carcinoma. Although its mechanism is not
known it appears to reduce the pain associated with HPOA

It has been used in the treatment of malignant bowel obstruction.[5]

Octreotide may be used in conjunction with midodrine to partially reverse peripheral vasodilation in the hepato-renal syndrome. By increasing systemic vascular resistance, these drugs reduce shunting and improve renal perfusion, prolonging survival until definitive treatment with liver transplant. [6]

M blocker block secretion and so cause dry mouth ipratropium
Ipratropium (Atrovent, Apovent) is an anticholinergic drug.[1] It blocks the muscarinic cholinergic receptors
in the smooth muscles of the bronchi in the lungs. This opens the bronchi, and provides relief in chronic
obstructive pulmonary disease.
Side effects
If ipratropium is inhaled, side-effects resembling those of other anticholinergics are minimal. However,
dry mouth and sedation have been reported. Also effects such as skin flushing, tachycardia, acute angle ocular
dislocure, nausea, palpitations and headache have been observed.

Albuterol (Salbutamol) is a short-acting ?2-adrenergic receptor agonist
Isoproterenol is a sympathomimetic beta adrenergic agonist medication.
It is structurally similar to epinephrine (adrenaline) but acts selectively on beta receptors, activating ?1
and ?2 receptors equally.[1]
Terbutaline (trade names Brethine, Bricanyl, or Brethaire) is a ?2-adrenergic receptor agonist, used as a
fast-acting bronchodilator (often used as a short-term asthma treatment) and as a tocolytic to delay premature
labour. The inhaled form of terbutaline starts working within 15 minutes and can last up to 6 hours.

Theophylline, also known as dimethylxanthine, is a methylxanthine drug used in therapy for respiratory diseases
such as COPD or asthma under a variety of brand names. Due to its numerous side-effects, these drugs are now
rarely administered for clinical use. As a member of the xanthine family, it bears structural and
pharmacological similarity to caffeine. It is naturally found in tea, although in trace amounts (~1 mg/L),[1]
significantly less than therapeutic doses.[2] It is found also in cocoa beans. Amounts as high as 3.7 mg/g have
been reported in Criollo cocoa beans.[3]

The main actions of theophylline involve:

relaxing bronchial smooth muscle
increasing heart muscle contractility and efficiency: positive inotropic
increasing heart rate: positive chronotropic
increasing blood pressure
increasing renal blood flow
some anti-inflammatory effects
central nervous system stimulatory effect mainly on the medullary respiratory center.

The oral drugs pioglitazone and rosiglitazone can cause or exacerbate heart failure and pulmonary edema and
should be avoided in patients with left ventricular dysfunction (impaired pumping ability of the heart) or
chronic renal insufficiency.
Rosiglitazone is an anti-diabetic drug in the thiazolidinedione class of drugs. It is marketed by the
pharmaceutical company GlaxoSmithKline as a stand-alone drug (Avandia) and in combination with metformin
(Avandamet) or with glimepiride (Avandaryl). Annual sales peaked at approx $2.5bn in 2006. The drug's patent
expires in 2012.[1]

Some reports have suggested that rosiglitazone is associated with a statistically significant risk of heart
attacks, but other reports have disagreed, and the controversy has not been resolved. Concern about adverse
effects has reduced the use of rosiglitazone despite its important and sustained effects on glycemic control.[2]

Like other thiazolidinediones (TZDs), the mechanism of action of rosiglitazone is through activation of the
intracellular receptor class of the peroxisome proliferator-activated receptors (PPARs), specifically PPAR?.
Rosiglitazone is a selective ligand of PPAR? and has no PPAR?-binding action.

Apart from its effect on insulin resistance, it appears to have an anti-inflammatory effect: nuclear factor
kappa-B (NF?B) levels fall and inhibitor (I?B) levels increase in patients on rosiglitazone.[3]

Side-effects and contraindications
A press release by GlaxoSmithKline in February 2007 noted that there is a greater incidence of fractures of the
upper arms, hands and feet in female diabetics given rosiglitazone compared with those given metformin or
glyburide.[8] The information was based on data from the ADOPT trial.[9] The same increase has been found with
pioglitazone (Actos), another TZD.

A meta-analysis reported in May 2007 that the use of rosiglitazone was associated with a significantly increased
risk of heart attack (odds ratio=1.43, (95% confidence interval, 1.03 to 1.98; P=0.03)), and an even higher risk
of death from all cardiovascular diseases (odds ratio=1.64).[10] The U.S. Food and Drug Administration (FDA)
issued an alert on May 21, 2007.[11] On July 30, 2007 an Advisory Committee of the Food and Drug Administration
concluded that the use of rosiglitazone for the treatment of type 2 diabetes was associated with a greater risk
of myocardial ischemic events (including heart attacks) than a placebo, but data from several long term,
prospective clinical trials showed that when rosiglitazone was compared to metformin, or sulfonylurea, there
was no difference in the risk of heart attack. This data, coupled with the meta-analysis, prompted the FDA to
state that the data on the association between rosiglitazone and myocardial ischemia were inconclusive. The
meta-analysis was not supported by an interim analysis of the trial designed to evaluate this, and several other
reports have failed to conclude the controversy. This weak evidence for adverse effects has dramatically reduced
the use of rosiglitazone, despite its important and sustained effects on glycemic control.[2]

In 2009 the RECORD study, an open label trial published in the Lancet, found that there was no increase in
cardiovascular hospitalisation or death with rosiglitazone compared to metformin plus sulfonylurea, but the
rate of heart failure causing admission to hospital or death was significantly increased.[12]

As early as September 2005, both Rosiglitazone and Pioglitazone have been suspected of causing Macular Edema,
which causes partial blindness in various spots of the angle of vision. While blindness is also a possible effect
of diabetes, which Rosiglitazone is intended to treat, an article in Canadian journal CMAJ has documented several
occurrences and recommends discontinuation at the first sign of vision problems. Both TZD's are contraindicated
in patients with NYHA Class III and IV heart failure.

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* Re:NBME 4 answer key?????
  arm999 - 09/08/10 18:41
  Form 4 BLOCK 1:

6-10 BEBDD
11-15 CEGBE
16-20 EDCIB (* 17-CORRECT IS "D")
21-25 HBABB (*24-CORRECT IS "B")
26-30 CDBEB
31-35 CBAAE
36-40 DJCBA
41-45 EFCCB
46-50 CGEBE

Form 4 BLOCK 2:

6-10 DADAD (*10-CORRECT IS "D")
11-15 EBAAB
16-20 DCDCA
21-25 FCDBD
26-30 CBDGA (*CORRECT ARE 26-C AND 28-D)
31-35 DECDD (*34-CORRECT IS "D")
36-40 FCEFC
41-45 DFBAD (* 45-CORRECT IS "D")
46-50 EBDCC

Form 4 BLOCK 3:

6-10 BBAEG
11-15 EAADC
16-20 EEAAA
21-25 BFAEE
26-30 CAFBA
31-35 EBAAB
36-40 DCFAD
41-45 BFABE
46-50 DBDDD

Form 4 BLOCK 4:

6-10 BABAF
11-15 AEABE (*12-CORRECT IS "E")
16-20 EADEA
21-25 ADEBE
26-30 BBDAH
31-35 EGEDA
36-40 AAGBC
41-45 CEDBE
46-50 ECCCB

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* Re:NBME 4 answer key?????
  abababab - 09/08/10 19:11
  Thanks guys  
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* Re:NBME 4 answer key?????
  freestep - 09/10/10 13:55
  Hi abababab:
Do you have a copy for NBME 5 and NBME 7. Can I have it from you. Thanks.
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* Re:NBME 4 answer key?????
  abababab - 09/10/10 16:38 (NBME 1-4) (NBME 6 and 7)

I got it from the links above. I got NBME 5 from someone else's post earlier. I dont remember. They are huge files and cannot be transferred over email. In case u are not able to download them from here give me ur skype ID
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* Re:NBME 4 answer key?????
  freestep - 09/10/10 19:00
  Hi abababab:
Thank you for posting the link. I got it. For the NBME 5, I wonder if you can put the link like this one. Can you please put The NBME 5 in the megaupload link. It is easy for me to down load. I don't have the Skyde ID (what is that by the way). Once again, thanks.
Have a nice day!
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* Re:NBME 4 answer key?????
  scanlojo - 12/29/17 05:19
  Could be wrong about this but is q25 from block one not B macular degeneration?  
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