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Old 03-29-2013
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Correct Answer NBME Form 7 Answer Key

hi guys.
I want to ask who took NBME 7. are these answers are right? i found them in this forum from a link. pleasee reply, I need to discuss some answers.

Block 1
____________
1-5 EABEA
6-10 BDABE
11-15 ABADG
16-20 AADBB
21-25 FDCED
26-30 FEDEA
31-35 GCBCA
36-40 BCBCA
41-45 FECAE
46-50 DABDE

Block 2
___________
1-5 AABBE
6-10 CEBAE
11-15 DDDBA
16-20 DECED
21-25 BBDDB
26-30 ADEDC
31-35 DDEEE
36-40 EEDAA
41-45 BDCDB
46-50 CDCBB

Block 3
___________
1-5 ACDEC
6-10 AEBDC
11-15 ACCBB
16-20 AEDBB
21-25 CBAAD
26-30 EBACA
31-35 ECBAD
36-40 DACAE
41-45 CABAB
46-50 DEDAE

Block 4
___________
1-5 AAADA
6-10 BEBDC
11-15 BABAE
16-20 CCFAA
21-25 EGBBA
26-30 DDBCC
31-35 AECFC
36-40 DCDDD
41-45 BBABB
46-50 CCADC
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Well it depends if u have the offline NBME that goes specifically with those answers.. Every NBME, taken online, is usually scrambled up.. So if ur NBME goes well with these choices, then it's probably correct.. If it's way off, then u might have a different offline version.. but in every answer choice found on the internet.. there will most likely be a few that are incorrect.. yea
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Quote:
Originally Posted by whatsupdoc86 View Post
Well it depends if u have the offline NBME that goes specifically with those answers.. Every NBME, taken online, is usually scrambled up.. So if ur NBME goes well with these choices, then it's probably correct.. If it's way off, then u might have a different offline version.. but in every answer choice found on the internet.. there will most likely be a few that are incorrect.. yea
I took online nbme 7 and I want to see my incorrect questions' answers. nbme doesnt release answers online. so how can I find?
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Correct Answer NBME 7 Answer with Detailed Explanations

NBME 7 BLOCK 1 answers

1. E. Rosuvastatin
- Statin decreases LDL
- Niacin increases HDL
- Fibrates decreases triaglycerides

HMG-coA reductase inhibitors are more effective for bringing the LDL to normal level....
They inhibit cholestrol precursor,Mevalonate
S/E...Rhabdomyolisis
reversible high level liver function test

Lovastatin,pravastatin,simvastatin,Atorvastatin,Ro sovastatin...........astatin

2. A. Bronchoconstriction

Zafirlucast,Montelucast.....Leukoterine receptor blockers prevent bronchoconstriction

3. B. “Do you know what kinds of foods are high in sodium?”

4. E. Primordial germ cell migration:

the tumor shows a haphazard arrangement of somatic tissues representing derivatives of ecto...,meso.. and endoderm.....it is a characteristic of germ cells.

Teratoma is derivative of primitive streak which involves process of germ cell migration.
- For number 4...This is a case of Sacrococcygeal teratoma..)....
- Sacrococcygeal teratoma is one of the extragonadal germ cell tumors ...
- These tumors can be found anywhere on the midline, particularly the
retroperitoneum, the anterior mediastinum, the sacrococcyx, and the pineal gland. Other
less common sites include the orbit, suprasellar area, palate, thyroid, submandibular region,
anterior abdominal wall, stomach, liver, vagina, and prostate. The classic theory suggests
that germ cell tumors (GCTs) in these areas are derived from local transformation of
primordial germ cells misplaced during embryogenesis...which means defect in primordial
germ cell migration

http://emedicine.medscape.com/article/278174-overview.....

My answer Is EE

F ... is for sacral agenesis… “Somite development”
D..is for spina bifida … “neural tube closure”
C..is for neurocristopathies, which include conditions such as frontonasal dysplasia,
Waardenburg-Shah syndrome, and DiGeorge syndrome, ......etc…”neural crest formation”
B..is clear…Hematopoiesis
A...is for cranial abnormalities.....”head mesenchyme proliferation”

5. A. Amitriptyline

Tricyclic antidepressant overdose....Tricyclics have a narrow therapeutic index, i.e., the therapeutic dose is close to the toxic dose.

The peripheral autonomic nervous system, central nervous system and the heart are the main systems that are affected following overdose.

Initial or mild symptoms typically develop within 2 hours and include tachycardia, drowsiness, a dry mouth, nausea and vomiting, urinary retention, confusion, agitation, and headache.
More severe complications include hypotension, cardiac rhythm disturbances, hallucinations, and seizures. Electrocardiogram (ECG) abnormalities are frequent and a wide variety of cardiac dysrhythmias can occur, the most common being sinus tachycardia and intraventricular conduction delay resulting in prolongation of the QRS complex and the PR/QT intervals.
Seizures, cardiac dysrhythmias, and apnea are the most important life threatening complications.[

6. B. Class II MHC molecule peptide loading

Professional APCs are very efficient at internalizing antigen, either by phagocytosis. The acidic compartments of macrophages are also responsible for the degradation of ingested micro-organisms) or by receptor-mediated endocytosis, and then displaying a fragment of the antigen, bound to a class II MHC molecule, on their membrane. The T cell recognizes and interacts with the antigen-class II MHC molecule complex on the membrane of the antigen-presenting cell.

7. D. Pyruvate carboxylase
- the problem is that she is hypoglycemia and then with an infusion w/ glucose, it helps.
- So the problem, is making glucose…hence, you need pyruvate carboxylase enzyme for gluconeogenesis.

A deficiency of pyruvate carboxylase can cause lactic acidosis as a result of lactate build up. Normally, excess pyruvate is shunted into gluconeogenesis via conversion of pyruvate into oxaloacetate, but because of the enzyme deficiency, excess pyruvate is converted into lactate instead.

As a key role of gluconeogenesis is in the maintenance of blood sugar, deficiency of pyruvate carboxylase can also lead to hypoglycemia

Pyruvate carboxylase is a mitochondria enzyme requiring biotin. It is activated by acetylCoA( from beta- oxidation. The product oxaloacetate(OAA), a citric acid cycle intermediate, cannot leave the mitochondria but is reduced to malate that can leave via a Malate shuffle. In the cytoplasm malate is reduced to (OAA).

Pyruvate carboxylase deficiency is an inherited disorder that causes lactic acid and other potentially toxic compounds to accumulate in the blood. High levels of these substances can damage the body's organs and tissues, particularly in the nervous system. Pyruvate carboxylase deficiency is a rare condition, with an estimated incidence of 1 in 250,000 births worldwide. This disorder appears to be much more common in some Algonkian Indian tribes in eastern Canada.
http://en.wikipedia.org/wiki/Pyruvat...ase_deficiency

8. A. Golgi complex

I-cell disease is an autosomal recessive disorder caused by a deficiency of GlcNAc phosphotransferase, which phosphorylates mannose residues to mannose-6-phosphate on N-linked glycoproteins in the Golgi apparatus within the cell.

Without mannose-6-phosphate to target them to the lysosomes, the enzymes are transported from the Golgi to the extracellular space, resulting in large intracellular inclusions of molecules requiring lysosomal degradation in patients with the disease .

The Golgi apparatus is unable to target the lysosomal protein (which is normal) to the lysosome. Without proper functioning of N-acetylglucosamine-1-phosphotransferase, a build up of substances occurs when enzymes are unable to travel inside of the lysosome

I- Cell Disease: (Inclusion cell disease). Inherited lysosomal storage disorder; failure of addition to mannose 6 phosphate to lysosome proteins( enzyme are secreted outside the cell instead of being targeted to the lysosme. Result in coarse facial future, clouded corneas, restricted join movement, and high plama levels of lysosomes. Often fatal childhood.
http://en.wikipedia.org/wiki/I-cell_disease

9. B. “I understand you concern. Let’s talk more about your specific worries.”

10. E. Neuromuscular junction

Myasthenia gravis is a chronic autoimmune neuromuscular disease characterized by varying degrees of weakness of the skeletal (voluntary) muscles of the body.

The hallmark of myasthenia gravis is muscle weakness that increases during periods of activity and improves after periods of rest. Certain muscles such as those that control eye and eyelid movement, facial expression, chewing, talking, and swallowing are often, but not always, involved in the disorder.

In myasthenia gravis, antibodies block, alter, or destroy the receptors for acetylcholine at the neuromuscular junction which prevents the muscle contraction from occurring

11. A. Decrease

Leuprolide: antagonist: pulsatile: treats prostate..meaning decrease LH/FSH.

http://en.wikipedia.org/wiki/Gonadot...easing_hormone

12. B. Centromere
a. Raynaud’s phenomenon…CREST syndrome…anti-centromere antibody

Crest Syndrome: Calcifications, Raynaud's phenomenon, Esophageal dysmotility, Sclerodactyly, and Telangiectasia. Limited skin involvement, often confined to fingers and face. More benign clinical course. Associated with Anticentromere Antibody.

13. A. Acute inflammation

Acute pancreatitis

14. C. D. Parvovirus B19

Two of the sources say that the answer is D. Parvovirus B 19 (maybe because it has to do with sickle cell anemia hence the hemoglobin & hematocrit is low but then wouldn’t you see sickle cell shape instead). Plus, parvovirus affect RBC precursors (reticulocytes), so, isn’t the ret ct kinda normal (since this is the case, you know that the bone marrow is working and it is compensation. E. Pneumocystis jiroveci (formerly P.carinii) is usually seen in adults.

AIDS
Parvovirus B19 is a cause of chronic anemia in individuals who have AIDS. It is frequently overlooked. Treatment with erythropoetin or intravenous immunoglobulin have been helpful in some patients. The parvovirus infection may trigger an inflammatory reaction in AIDS patients who have just begun antiretroviral therapy.[14].

http://en.wikipedia.org/wiki/Parvovirus_B19

15. G. Parathorone-related protein

When associated with the lung, it often causes ectopic production of parathyroid hormone-related protein (PTHrP), resulting in hypercalcemia.

Squamous-cell carcinoma of the lung is more common in men than in women. It is closely correlated with a history of tobacco smoking, more so than most other types of lung carcinoma. It most often arises centrally in larger bronchi, and while it often metastasizes to locoregional lymph nodes (particularly the hilar nodes) early in its course, it generally disseminates outside the thorax somewhat later than other major types. Large tumors may undergo central necrosis, resulting in cavitation. A squamous-cell carcinoma is often preceded for years by squamous-cell metaplasia or dysplasia in the respiratory epithelium of the bronchi, which later transforms to carcinoma in situ. In carcinoma in situ, atypical cells may be identified by cytologic smear test of sputum, bronchoalveolar lavage or samples from endobronchial brushings. However, squamous-cell carcinoma in situ is asymptomatic and undetectable on X-ray radiographs. Eventually, it becomes symptomatic, usually when the tumor mass begins to obstruct the lumen of a major bronchus, often producing distal atelectasis and infection. Simultaneously, the lesion invades into the surrounding pulmonary substance. On histopathology, these tumors range from well-differentiated, showing keratin pearls and cell junctions, to anaplastic with only minimal residual squamous-cell features.
http://en.wikipedia.org/wiki/Squamous-cell_carcinoma

16. A. Alkaline phosphatase activity

Paget's disease may be diagnosed using one or more of the following tests:

Pagetic bone has a characteristic appearance on X-rays. A skeletal survey is therefore indicated.

http://upload.wikimedia.org/wikipedi...gets_skull.jpg

An elevated level of alkaline phosphatase in the blood in combination with normal calcium, phosphate, and aminotransferase levels in an elderly patient are suggestive of Paget's disease.
Bone scans are useful in determining the extent and activity of the condition. If a bone scan suggests Paget's disease, the affected bone(s) should be X-rayed to confirm the diagnosis

The pathogenesis of Paget's disease is described in 3 stages, which are:
i. Osteoclastic activity
ii. Mixed osteoclastic-osteoblastic activity
iii. Exhaustive (burnt out) stage


Initially, there is a marked increase in the rate of bone resorption at localized areas caused by large and numerous osteoclasts. These localized areas of osteolysis are seen radiologically as an advancing lytic wedge in long bones or osteoporosis circumscripta in the skull. The osteolysis is followed by a compensatory increase in bone formation induced by osteoblasts recruited to the area. This is associated with accelerated deposition of lamellar bone in a disorganized fashion. This intense cellular activity produces a chaotic picture of trabecular bone ("mosaic" pattern), rather than the normal linear lamellar pattern. The resorbed bone is replaced and the marrow spaces are filled by an excess of fibrous connective tissue with a marked increase in blood vessels, causing the bone to become hypervascular. The bone hypercellularity may then diminish, leaving a dense "pagetic bone," also known as burned-out Paget's disease.

17. A. Discuss comfort care with the patient’s wife

all choices except A are artificial procedures that prolong his life.

18. D. Schistocytes

Normal lactate dehydrogenase is 25-90 U/L…this patient has 1000 U/L..definitely TTP

TTP: Thrombotic Thrombocytopenia Purpura: is a rare disorder of the blood-coagulation system, causing extensive microscopic thromboses to form in small blood vessels throughout the body (thrombotic microangiopathy). Most cases of TTP arise from inhibition of the enzyme ADAMTS13, a metalloprotease responsible for cleaving large multimers of von Willebrand factor (vWF) into smaller units. A rarer form of TTP, called Upshaw-Schülman syndrome, is genetically inherited as a dysfunction of ADAMTS13. If large vWF multimers persist there is tendency for increased coagulation.

http://en.wikipedia.org/wiki/Thrombo...openic_purpura

TPP: FA page 349) Symptoms: pentada of neurologic and renal symptoms, fever, thrombocytopenia, and microangiopathic hemolytic anemia.
Lab: Schistocytes, increase LDH.

19. B. GM2-ganglioside

Tay sach disease: AR, Progresive neurodegeneration, developmental delay, cherry red spot on macula, lysosomal with onion skin , NO HEPATOMEGALY. Def. enzime: Hexosaminidase A; Accumulated substrate: G2 ganglioside. (FA page 111).

20. B. Smell

Olfatory CN I is the only CN without thalamic relay to cortex. Function: Smell ( FA 413)

21. F. Increased volume of distribution

22. D. Pneumothorax

Pneumothorax is defined as the presence of air or gas in the pleural cavity, that is, in the potential space between the visceral and parietal pleura of the lung. The result is collapse of the lung on the affected side. Air can enter the intrapleural space through a communication from the chest wall (ie, trauma) or through the lung parenchyma across the visceral pleura.

Primary spontaneous pneumothorax (PSP) occurs in people without underlying lung disease and in the absence of an inciting event . In other words, air is present in the intrapleural space without preceding trauma and without underlying clinical or radiologic evidence of lung disease.

Risks factors for primary spontaneous pneumothorax (PSP) include the following:

•Smoking
•Tall, thin stature in a healthy person
•Marfan syndrome
•Pregnancy
•Familial pneumothorax
Blebs and bullae (sometimes called emphysematouslike changes or ELCs) are related to the occurrence of primary spontaneous pneumothorax.


Secondary spontaneous pneumothorax (SSP) occurs in people with a wide variety of parenchymal lung diseases, that is, these individuals have underlying pulmonary structural pathology (see the image below). Air enters the pleural space via distended, damaged, or compromised alveoli. Patients may present with more serious clinical symptoms and sequelae due to comorbid conditions.

Diseases and conditions associated with secondary spontaneous pneumothorax include the following:

•Chronic obstructive lung disease (COPD) or emphysema: Increased pulmonary pressure due to coughing with a bronchial plug of mucus or phlegm bronchial plug may play a role.
•Asthma
•Human immunodeficiency virus/acquired immunodeficiency syndrome (HIV/AIDS) with PCP infection
•Necrotizing pneumonia
•Tuberculosis
•Sarcoidosis
•Cystic fibrosis
•Bronchogenic carcinoma or metastatic malignancy
•Idiopathic pulmonary fibrosis
•Inhalational and intravenous drug use (eg, marijuana, cocaine)[8]
•Interstitial lung diseases associated with connective tissue diseases
•Lymphangioleiomyomatosis
•Langerhans cell histiocytosis
•Severe acute respiratory syndrome (SARS): A reported 1.7% of SARS patients developed spontaneous pneumothorax.
•Thoracic endometriosis and catamenial pneumothorax
•Collagen vascular disease, including Marfan syndrome


23. C. Ganciclovir

Ganciclovir is an antiviral medication used to treat or prevent cytomegalovirus (CMV) infections
It is first phosphorylated to a deoxyguanosine triphosphate (dGTP) analogue. This competitively inhibits the incorporation of dGTP by viral DNA polymerase, resulting in the termination of elongation of viral DNA.

Adverse effects:
Ganciclovir is commonly associated with a range of serious haematological adverse effects. granulocytopenia, neutropenia, anaemia, thrombocytopenia, fever, nausea, vomiting, dyspepsia, diarrhoea, increased serum creatinine and blood urea concentrations

Toxicity:

Ganciclovir is considered a potential human carcinogen, teratogen, and mutagen. It is also considered likely to cause inhibition of spermatogenesis. Thus, it is used judiciously and handled as a cytotoxic drug in the clinical setting

24. E. Mitral regurgitation

Holosystolic murmur is best heard at the apex in the left lateral decubitus position....Mitral Regurgitation .

Murmur:

Blowing holosystolic murmur
Heard best at the apex
Radiation to the axilla and inferior edge of left scapula.
Possible associated findings:

S2: wide physiologic splitting
S3

http://depts.washington.edu/physdx/heart/tech.html

25. D. Rest (systolic < diastolic) vs. Moderate exercise (systolic < diastolic)
- the cardiac cycle where by coronary arteries deliver oxygen to the myocardium is during diastole........whether it is systolic or diastolic.....this is my assumption.
- no matter if the person is at rest or doing exercise, the coronary blood flow is always more during diastole. although the duration of flow is greatest during rest as oppose to exercise when the heart rate is faster and thus diastole is of less duration.

Coronary blood flow occurs mostly during diastole, because during systole the blood vessels within the myocardium are compressed. Increased heart rates, which reduce the time for diastole filling, can reduce the myocardial blood supply and cause ischemia.

Dynamic exercise increases coronary blood flow in proportion to the heart rate, with peak values during maximal exercise typically three to five times the resting level .

26. F. Surfactant

Severely premature infants may have underdeveloped lungs, because they are not yet producing their own surfactant. This can lead directly to respiratory distress syndrome, also called hyaline membrane disease, in the neonate.

To try to reduce the risk of this outcome, pregnant mothers with threatened premature delivery prior to 34 weeks are often administered at least one course of glucocorticoids, a steroid that crosses the placental barrier and stimulates the production of surfactant in the lungs of the fetus.

27. E. Increase B-hydroxybutyrate; increase osmality; increase anion gap

- Case of diabetic ketoacidosis...high glucose ...high ketones
- Betahydroxy butyrate and acetoacetate both increase.....
- Osmolarity =2 Serum Na+serum glucose /18+BUN/2.8 ...so if u increase glucose u increase
plasma osmolarity
- Anion Gap = Serum Na - (serum Chloride + Serum HCO3)...in the case of diabetic Ketoacidosis
- anions of acid (acetoacetate and beta hydroxybutyrate) replace HCO3 ...hence we only subtract Chloride from the Serum Na ...that makes the anion gap to increase....

n DKA
*beta-Hydroxybutyric acid is a ketone body....inc
*Due to loss of water......inc. serum osmolality.
*The anion gap is the difference in the measured cations and the measured anions in serum, plasma, or urine. The magnitude of this difference (i.e. "gap") in the serum is often calculated in medicine when attempting to identify the cause of metabolic acidosis.

only Na+, Cl− and HCO3− (+/- K) are used when calculating the anion gap... healthy adults is 8-12 mEq/L

( [Na+] ) − ( [Cl−]+[HCO3−] )

a useful mnemonic to remember the high anion gap is MUDPILES (methanol, uremia, diabetic ketoacidosis, propylene glycol, isoniazid, lactic acidosis, ethylene glycol, salicylates).


28. D. Pseudomonas aeruginosa

It is a Gram-negative, aerobic, rod-shaped bacterium with unipolar motility and oxidase positive

P. aeruginosa secretes a variety of pigments, including pyocyanin (blue-green),
Because it thrives on most surfaces, this bacterium is also found on and in medical equipment, including catheters, causing cross-infections in hospitals and clinics. It is implicated in hot-tub rash.

29. E. Mitral valve prolapse

Marfan syndrome can lead to mitral valve prolapse (MVP)

30. A. Increase hemoglobin F; increase Hemoglobin A2: hemoglobin A ratio; increase reticulocyte count
- Patient has beta thalassemia
o Normal adult hemoglobin is alpha 2, beta 2, and alpha 2, gamma 2
o Increase HbA2 (>3.5%)
• You compare the ratio of Adult 2 with Adult 1
• Adult 2 is normal, hence, adult 2 has a higher normal adult hemoglobin than Adult 1
o Both major & minor = increase HbF (alpha 2; gamma 2)
• Adult 1 normally has alpha 2, beta 2
• Adult 2 normally has alpha 2, delta 2
• In beta thalassemia, you change beta 2 in adult 1 with HbF (alpha 2, gamma 2)
• So, now, the adult 1 has alpha 2, HbF…aka alpha 2, gamma 2
• Hence, you see an increase in HbF
o Reticulytes is normal/to increase because there is nothing wrong with the bone marrow so therefore, it doesn’t the reticulocytes.
o embryonic hemoglobin: 2z, 2e
o transition hemoglobin: 2z, 2y
o fetal hemoglobin: 2alpha, 2y
o adult hemoglobin HbA1: 2 alpha, 2 beta
o adult 2: 2 alpha, 2 delta

Beta thalasemia: prevalent in mediterranea population.
Defect: point mutation in splicing sites and promoter sequences
Beta thalasemia minor (heterozygote)
1. beta chain in unproduced
2. usually asyntomptomatic
3. Dx confirmed by increase HbA2 ( > 3.5%)
Beta thalasemia major: (Homozygote)
1. beta chain is absent- severe anemia requiring blood transfusion (2º hemochromatosis)
2. Marrow expansion ( crew cut on skull x-ray)- skeletal defromities, chipmunk facies
Both major and minor - increase Hb F (FA page 343).

31. G. B2 adrenergic agonist

Beta 2 adrenergic agonist: Bronchodilation (relax bronchial smooth mucles)

32. C. Thyroid-stimulating hormone

TSH: Thyroid-stimulating hormone (also known as TSH or thyrotropin) is a peptide hormone synthesized and secreted by thyrotrope cells in the anterior pituitary gland, which regulates the endocrine function of the thyroid gland. TSH is the 1st step in evaluation of thyroid function.

33. B. Adenocarcinoma of the endometrium

Adenocarcinoma of the endometrium:
Carcinoma endometrial is the Most common gynecologic malignancy. peak occurrence at 55-65 year of age. Clinically presents with vaginal bleeding. Typically proceeded by endometrial hyperplasia. Risk factors include prolonged use of estrogen without progestins, obesity, diabetes, hypertension, nulliparity and late menopause. Increase myometrial invasion, decrease prognosis. (FA page 487)

34. C. Globus pallidus

Parkinson disease
Surgery and deep brain stimulation
Placement of an electrode into the brain. The head is stabilized in a frame for stereotactic surgery. Treating motor symptoms with surgery was once a common practice, but since the discovery of levodopa, the number of operations declined. Studies in the past few decades have led to great improvements in surgical techniques, so that surgery is again being used in people with advanced PD for whom drug therapy is no longer sufficient.[35] Surgery for PD can be divided in two main groups: lesional and deep brain stimulation (DBS). Target areas for DBS or lesions include the thalamus, the globus pallidus or the subthalamic nucleus.[35] Deep brain stimulation (DBS) is the most commonly used surgical treatment. It involves the implantation of a medical device called a brain pacemaker, which sends electrical impulses to specific parts of the brain. DBS is recommended for people who have PD who suffer from motor fluctuations and tremor inadequately controlled by medication, or to those who are intolerant to medication, as long as they do not have severe neuropsychiatric problems.[29] Other, less common, surgical therapies involve the formation of lesions in specific subcortical areas (a technique known as pallidotomy in the case of the lesion being produced in the globus pallidus).[35]

35. A. Deep fibular (peroneal)

PED: peroneal; eversion; dorsiflexion

Deep Fibular nerve: Weakness inversion, Loss extension of the digits, loss dorsiflexion ( foot drop), sensory loss on antero lateral leg and dorso of the foot, first web space. (Kaplan anatomy page 295 and 295)

36. B. Placenta accrete

Placeta accreta: An invasion of the myometrium which does not penetrate the entire thickness of the muscle. This form of the condition accounts for around 75% of all cases.

Placenta perccreta: The worst form of the condition is when the placenta penetrates the entire myometrium to the uterine serosa (invades through entire uterine wall). This variant can lead to the placenta attaching to other organs such as the rectum or bladder[1

37. C. Ileum

Crohn Disease: Also known as regional enteritis, is an inflammatory disease of the intestines that may affect any part of the gastrointestinal tract from mouth to anus, causing a wide variety of symptoms. It primarily causes abdominal pain, diarrhea (which may be bloody if inflammation is at its worst), vomiting, or weight loss,[1][2][3] but may also cause complications outside the gastrointestinal tract such as skin rashes, arthritis, inflammation of the eye, tiredness, and lack of concentration.[1]

Crohn's disease is thought to be an autoimmune disease, in which the body's immune system attacks the gastrointestinal tract, causing inflammation; it is classified as a type of inflammatory bowel disease. There is evidence of a genetic link to Crohn's disease, putting individuals with siblings afflicted with the disease at higher risk.[4] It is thought to have a large environmental component as evidenced by a higher incidence in western industrialized nations compared to other parts of the world. Males and females are equally affected. Smokers are two times more likely to develop Crohn's disease than.

http://en.wikipedia.org/wiki/Crohn's_disease.
Gross morphology: transmural inflamation, Cobblestone mucosa, creeping fat, bowell wall thickning, (string sign on barium swallow x- ray) linear, ulcers, fissures, fistulas.
Microscopic morphology: Noncaseating granulomasand lymphoid

38. B. 0.19

positive predictive value Positive (PPV): TP/ (TP+FP)
PPV= 70/(70+300)= 0.18 in this case aprox. 0.19

39. C. Membranous nephropathy

Membranous Glomerulonephritis: LM -diffuse capillary and GBM thickening. EM " spike and dome" appearance with subepithelial deposits. IF - granular.

Caused by drugs ( penicillamine, Gold, NSAID). Most common cause of adult nephrotic syndrome.
The closely related terms membranous nephropathy[1] and membranous glomerulopathy[2] both refer to a similar constellation but without the assumption of inflammation.

Some patients may present as nephrotic syndrome with proteinuria, edema with or without renal failure. Others may be asymptomatic and may be picked up on screening or urinalysis as having proteinuria. A definitive diagnosis of membranous nephropathy requires a kidney biopsy.



40. A. Esctasy (3,4-methylenedioxymethamphetamine)

Intoxication for Amphetamine: Psychomotor agitation , impaired judgment, pupillary dilation, hypertension, tachycardia, euphoria, prolonged weakfulness sand attention, cardiac arrythmia, delusions, hallucinations, fever. (FA 448)

Amphetamine: Blocks of neurotransmiter uptake at the presynaptic nerve terminal

41. F. Tronchanteric bursa

- Trochanteric bursitis is characterized by painful inflammation of the bursa located just superficial to the greater trochanter of the femur. Patients typically complain of lateral hip pain, although the hip joint itself is not involved. The pain may radiate down the lateral aspect of the thigh.
- The term greater trochanteric pain syndrome (GTPS) is now being commonly substituted for trochanteric bursitis, because the inflammatory etiology of the pain is being refuted by current research, using ultrasonographic, magnetic resonance imaging (MRI) – based, and histologic evidence.
- Flexion or anteversion (140°): iliopsoas (with psoas major from vertebral column); tensor fascia latae, pectineus, adductor longus, adductor brevis, and gracilis. Thigh muscles acting as hip flexors: rectus femoris and sartorius.

42. E. X-linked recessive

Duchenne muscular dystrophy (DMD) is a recessive X-linked. The disorder is caused by a mutation in the dystrophin gene, located in humans on the X chromosome (Xp21). The dystrophin gene codes for the protein dystrophin, an important structural component within muscle tissue.

43. C. Medial collateral ligament

Medial collateral ligament" known as the tibial collateral ligament too.MCL strains and tears are fairly common in American football. Mostly the center and the guards are ones who get this injury, due to the grip trend on their cleats.

An MCL injury can be very painful and is caused by a valgus stress to a slightly bent knee, often when landing, bending or on high impact. Depending on the grade of the injury, the lowest grade (grade 1) can take between 2 and 10 weeks for the injury to fully heal. Recovery times for grades 2 and 3 are difficult to predict because of the amount of damage done can take weeks to several months. It is difficult to apply pressure on the injured leg for at least a few days.

44. A. They attributed the difference in success rates to chance alone

In order for it to be stagistical significance, you need the P value to be 0.05 aka 95%

But since the P value here is 0.3 aka 70%..it is only due to chance.

The P value for a study should be less than 0.05.

This value means that when we perform a study, the 95% of the time the observations are rite & 5 % of the time the observation are due to chance alone.

In this question the value of P is 0.3 which means that the probability that these observations are due to chance alone is 30%, which is not a statistically acceptable number.

45. E. St. John’s wort

St John's wort has been shown to cause multiple drug interactions through induction of the cytochrome P450 enzyme CYP3A4, but also CYP2C9. This results in the increased metabolism of those drugs, resulting in decreased concentration and clinical effect.
Examples of drugs causing clinically-significant interactions with St John's wort
Class Drugs
antiretrovirals non-nucleoside reverse transcriptase inhibitors, protease inhibitors
benzodiazepines alprazolam, midazolam
hormonal contraception combined oral contraceptives
immunosuppressants calcineurin inhibitors, ciclosporin, tacrolimus
others, digoxin, methadone, omeprazole, phenobarbitol, theophylline, warfarin, levodopa, suboxone, Irinotecan

46. D. Increased osmolarity in the tubular lumen (urine)
o the boy has DM type 1
o in type 1 you have high glucose, no insulin
o high glucose will reabsorb all of the water into the cells, this pull water away from the tubule (urine) and you get hypertonic urine

http://en.wikipedia.org/wiki/Diabetic_ketoacidosis

Osmotic diuresis is increased urination caused by the presence of certain substances in the small tubes of the kidneys.[1] The excretion occurs when substances such as glucose enter the kidney tubules and cannot be reabsorbed (due to a pathological state or the normal nature of the substance). The substances cause an increase in the osmotic pressure within the tubule, causing retention of water within the lumen, and thus reduces the reabsorption of water, increasing urine output (ie. diuresis). The same effect can be seen in therapeutics such as mannitol, which is used to increase urine output and decrease extracellular fluid volume.
Substances in the circulation can also increase the amount of circulating fluid by increasing the osmolarity of the blood. This has the effect of pulling water from the interstitial space, making more water available in the blood and causing the kidney to compensate by removing it as urine. In hypotension, often colloids are used intravenously to increase circulating volume in themselves, but as they exert a certain amount of osmotic pressure, water is therefore also moved, further increasing circulating volume. As blood pressure increases, the kidney removes the excess fluid as urine.
Sodium, chloride, potassium are excreted in Osmotic diuresis, originating from Diabetes Mellitus (DM). Osmotic diuresis results in dehydration from polyuria and the classic polydipsia (excessive thirst) associated with DM.
http://en.wikipedia.org/wiki/Osmotic_diuresis

47. A. 312
- CPM ...stands for count per minute ..which is a measure of radioactivity. It is the number of
atoms in a given quantity of radioactive material that are detected to have decayed in one
minute.
- Mixed Lymphocyte Reaction... a test used to check class II compatibilty testing ...in this test
lymphocytes from one individual being tested(donor ) are irradiated so that they cant proliferate..
but will act as a stimulator cells for the presentation of MHC antigens ...the other individual
cells (Recipient) are added to the culture ,and uptake of tritiated thymidine is used as an
indicator of cell proliferation....if the MHC class II antigens are different ,proliferation will
occur ..if they are the same, no proliferation will occurr....
- Proliferation is directly proportional to CPM
- high CPM .....high proliferation....MHC II different ...not compatible
- low CPM ...less proliferation...MHC II similar...less risk of rejection....compatible

MLR lymphocytes from the donor and recipient are mixed and allowed to react. If they are compatible there will not be stimulation and the lymphocyte may not proliferate, some lymphocytes will degenerate and the count will reduce, if they are not compatible the donor lymphocte will be stimulated and will start to proliferate with a increased count. You can see the only count that is smaller thean the host is 312.

if they are not compatible and the lymphocytes are activated and start proliferating, the donor lymphocytes will be outnumbered... the point is that you don't want the donor lymphocytes to proliferate at a higher rate than the guy's own...

http://books.google.com/books?id=EJX......ion&f=false

In this test, "stimulator" lymphocytes from a potential donor are first killed by irradiation and then mixed with live "responder" lymphocytes from the recipient; the mixture is incubated in cell culture to permit DNA synthesis, which is measured by incorporation of tritiated thymidine. The greater the amount of DNA synthesis in the responder cells, the more foreign are the class II MHC proteins of the donor cells. A large amount of DNA synthesis indicates an unsatisfactory "match"; i.e., donor and recipient class II (HLA-D) MHC proteins are not similar, and the graft is likely to be rejected. The best donor is, therefore, the person whose cells stimulated the incorporation of the least amount

48. B. Acidification causing increased ammonium ion excretion

Ammonium is basic, hence, to excrete it, you need to acidifiy it.

Lactulose inhibits bacterial ammonia production by acidifying the content of the bowel. It promotes growth of colonic flora. The growing biomass uses ammonia and nitrogen from amino acids to synthesise bacterial protein, which in turn inhibits protein degradation to NH3. Lactulose leads to less ammonia by inhibiting bacterial urea degradation and reduces colonic transit time, thus reducing the time available for ammonia production and expediting ammonia elimination.

49. D. Metaplasia of the esophageal epithelium
This is a case of GERD...with esophagitis for the last 8 months...
Gastroesophageal reflux disease (GERD) occurs when the amount of gastric juice that
refluxes into the esophagus exceeds the normal limit, causing symptoms with or without
associated esophageal mucosal injury (ie, esophagitis).
Pathogenesis of GERD...Transient relaxation of LES and Ineffective esophageal clearance of
reflux material (bile acid and gastric juice)...hence the amount of acid that is secreted by the
stomach doesnt have any significant effect ...also whether there is H pylori or not has no
significance ...as well as whether the stomach is atrophic or not ...

Hence I go for metaplasia of the esophageal epithelium (given the 8 month history )

Barrett's esophagus is a condition in which the normal squamous epithelium of the esophagus has been replaced by an abnormal red columnar epithelium called specialized intestinal metaplasia. Specialized intestinal metaplasia is red, like normal stomach tissue, but does not look like stomach tissue under the microscope.

50. E. urolithiasis

- acidic, low protein in the fluid meaning that the (normal protein is 1.02); blood 4+ (lots of hemolysis…so think RBC cast); glucose is negative is it is not bacteria bc bacteria takes up glucose; bilirubin is negative so it is not the liver problem; leukocyte esterase negative so it can’t be E. Coli;
o B. Nodular prostatic hyperplasia is not the answer because he is too you and he doesn’t alkaline phosphtase increase
o C. RCC is not it because RCC is chronic…this guy has acute
o D. Schistomoasis…is a worm..so you should see a present of eosophil…and plus this patient glucose is negative. F

Urolithiasis is the condition where urinary calculi are formed in the urinary tract.

Most common kidney stons...Calcium Oxalate,Calcium phosphate,or both...Radiopaque
Oxalate crystal..result fromEthylen glycol
Secound most common....Ammonium Magnesium phosphate..Struvite....caused by infecction with Urease-positive bugs.......can form staghorn calculi

Uric acid....associated with hyperuricemia........readiolucent

Cysteine...secondary to Cystinuria..Hexogonal shape.........faintly radiopaque...treat with alkalization

In some cases, kidney stones pass out of the body without producing any symptoms. Most kidney stones, however, do cause some symptoms. The most common symptom from kidney stones is pain. The pain from kidney stones is a result of the stone getting stuck on its way out.

If fever and chills accompany any of these symptoms, an infection may be present and medical attention is needed sooner rather than late.

Laboratory Testing:
Laboratory testing includes urinalysis to detect the presence of blood (hematuria) and bacteria (bacteriuria) in the urine.
Other tests include blood tests for creatinine (to evaluate kidney function), BUN and electrolytes to detect dehydration, calcium to detect hyperparathyroidism, and a complete blood count to detect infection.

X-rays: A standard x-ray of the kidney, ureter, and bladder, may be adequate as a first step for identifying many stones since most are visible on x-ray.

Ultrasound: This test uses high frequency sound waves to produce pictures. Ultrasounds can detect a dilated kidney and ureter caused by a stone lodged in the ureter. Ultrasound, however, cannot reliably detect all stones especially stones located outside the kidney. It is the preferred imaging method for kidney stone patients who are pregnant.

IVP (Intravenous Pyelogram): For an IVP, a special dye is injected into the patient's veins. The dye collects in the urinary system and produces a white shadow when an x-ray is taken. The dye allows to precisely locate the stone and to determine the condition of the kidneys and ureters. Most kidney stones can be precisely located using this procedure.

CT Scan (Computerized Tomography): This test uses a scanner and a computer to create images of the urinary system. A CT scan done to look for kidney stones does not use contrast material. It is the most common imaging test used today to evaluate a possible kidney stone attack.
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  #5  
Old 03-30-2013
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hi insomniac. do you have the detailed answers of form 6/11/12/13? if u have any ..please do post the link. It'll be a great help.
thank you.
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Old 03-31-2013
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thanks insomniac
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Old 05-25-2013
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Insomniac thanks a lot for the post! do you have explanations for the other blocks from form 7? thanks!
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Default Ask for answer of other blocks of form 7

Many thanks!!
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  #9  
Old 04-21-2014
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Quote:
Originally Posted by Insomniac View Post
NBME 7 BLOCK 1 answers

1. E. Rosuvastatin
- Statin decreases LDL
- Niacin increases HDL
- Fibrates decreases triaglycerides

HMG-coA reductase inhibitors are more effective for bringing the LDL to normal level....
They inhibit cholestrol precursor,Mevalonate
S/E...Rhabdomyolisis
reversible high level liver function test

Lovastatin,pravastatin,simvastatin,Atorvastatin,Ro sovastatin...........astatin

2. A. Bronchoconstriction

Zafirlucast,Montelucast.....Leukoterine receptor blockers prevent bronchoconstriction

3. B. “Do you know what kinds of foods are high in sodium?”

4. E. Primordial germ cell migration:

the tumor shows a haphazard arrangement of somatic tissues representing derivatives of ecto...,meso.. and endoderm.....it is a characteristic of germ cells.

Teratoma is derivative of primitive streak which involves process of germ cell migration.
- For number 4...This is a case of Sacrococcygeal teratoma..)....
- Sacrococcygeal teratoma is one of the extragonadal germ cell tumors ...
- These tumors can be found anywhere on the midline, particularly the
retroperitoneum, the anterior mediastinum, the sacrococcyx, and the pineal gland. Other
less common sites include the orbit, suprasellar area, palate, thyroid, submandibular region,
anterior abdominal wall, stomach, liver, vagina, and prostate. The classic theory suggests
that germ cell tumors (GCTs) in these areas are derived from local transformation of
primordial germ cells misplaced during embryogenesis...which means defect in primordial
germ cell migration

http://emedicine.medscape.com/article/278174-overview.....

My answer Is EE

F ... is for sacral agenesis… “Somite development”
D..is for spina bifida … “neural tube closure”
C..is for neurocristopathies, which include conditions such as frontonasal dysplasia,
Waardenburg-Shah syndrome, and DiGeorge syndrome, ......etc…”neural crest formation”
B..is clear…Hematopoiesis
A...is for cranial abnormalities.....”head mesenchyme proliferation”

5. A. Amitriptyline

Tricyclic antidepressant overdose....Tricyclics have a narrow therapeutic index, i.e., the therapeutic dose is close to the toxic dose.

The peripheral autonomic nervous system, central nervous system and the heart are the main systems that are affected following overdose.

Initial or mild symptoms typically develop within 2 hours and include tachycardia, drowsiness, a dry mouth, nausea and vomiting, urinary retention, confusion, agitation, and headache.
More severe complications include hypotension, cardiac rhythm disturbances, hallucinations, and seizures. Electrocardiogram (ECG) abnormalities are frequent and a wide variety of cardiac dysrhythmias can occur, the most common being sinus tachycardia and intraventricular conduction delay resulting in prolongation of the QRS complex and the PR/QT intervals.
Seizures, cardiac dysrhythmias, and apnea are the most important life threatening complications.[

6. B. Class II MHC molecule peptide loading

Professional APCs are very efficient at internalizing antigen, either by phagocytosis. The acidic compartments of macrophages are also responsible for the degradation of ingested micro-organisms) or by receptor-mediated endocytosis, and then displaying a fragment of the antigen, bound to a class II MHC molecule, on their membrane. The T cell recognizes and interacts with the antigen-class II MHC molecule complex on the membrane of the antigen-presenting cell.

7. D. Pyruvate carboxylase
- the problem is that she is hypoglycemia and then with an infusion w/ glucose, it helps.
- So the problem, is making glucose…hence, you need pyruvate carboxylase enzyme for gluconeogenesis.

A deficiency of pyruvate carboxylase can cause lactic acidosis as a result of lactate build up. Normally, excess pyruvate is shunted into gluconeogenesis via conversion of pyruvate into oxaloacetate, but because of the enzyme deficiency, excess pyruvate is converted into lactate instead.

As a key role of gluconeogenesis is in the maintenance of blood sugar, deficiency of pyruvate carboxylase can also lead to hypoglycemia

Pyruvate carboxylase is a mitochondria enzyme requiring biotin. It is activated by acetylCoA( from beta- oxidation. The product oxaloacetate(OAA), a citric acid cycle intermediate, cannot leave the mitochondria but is reduced to malate that can leave via a Malate shuffle. In the cytoplasm malate is reduced to (OAA).

Pyruvate carboxylase deficiency is an inherited disorder that causes lactic acid and other potentially toxic compounds to accumulate in the blood. High levels of these substances can damage the body's organs and tissues, particularly in the nervous system. Pyruvate carboxylase deficiency is a rare condition, with an estimated incidence of 1 in 250,000 births worldwide. This disorder appears to be much more common in some Algonkian Indian tribes in eastern Canada.
http://en.wikipedia.org/wiki/Pyruvat...ase_deficiency

8. A. Golgi complex

I-cell disease is an autosomal recessive disorder caused by a deficiency of GlcNAc phosphotransferase, which phosphorylates mannose residues to mannose-6-phosphate on N-linked glycoproteins in the Golgi apparatus within the cell.

Without mannose-6-phosphate to target them to the lysosomes, the enzymes are transported from the Golgi to the extracellular space, resulting in large intracellular inclusions of molecules requiring lysosomal degradation in patients with the disease .

The Golgi apparatus is unable to target the lysosomal protein (which is normal) to the lysosome. Without proper functioning of N-acetylglucosamine-1-phosphotransferase, a build up of substances occurs when enzymes are unable to travel inside of the lysosome

I- Cell Disease: (Inclusion cell disease). Inherited lysosomal storage disorder; failure of addition to mannose 6 phosphate to lysosome proteins( enzyme are secreted outside the cell instead of being targeted to the lysosme. Result in coarse facial future, clouded corneas, restricted join movement, and high plama levels of lysosomes. Often fatal childhood.
http://en.wikipedia.org/wiki/I-cell_disease

9. B. “I understand you concern. Let’s talk more about your specific worries.”

10. E. Neuromuscular junction

Myasthenia gravis is a chronic autoimmune neuromuscular disease characterized by varying degrees of weakness of the skeletal (voluntary) muscles of the body.

The hallmark of myasthenia gravis is muscle weakness that increases during periods of activity and improves after periods of rest. Certain muscles such as those that control eye and eyelid movement, facial expression, chewing, talking, and swallowing are often, but not always, involved in the disorder.

In myasthenia gravis, antibodies block, alter, or destroy the receptors for acetylcholine at the neuromuscular junction which prevents the muscle contraction from occurring

11. A. Decrease

Leuprolide: antagonist: pulsatile: treats prostate..meaning decrease LH/FSH.

http://en.wikipedia.org/wiki/Gonadot...easing_hormone

12. B. Centromere
a. Raynaud’s phenomenon…CREST syndrome…anti-centromere antibody

Crest Syndrome: Calcifications, Raynaud's phenomenon, Esophageal dysmotility, Sclerodactyly, and Telangiectasia. Limited skin involvement, often confined to fingers and face. More benign clinical course. Associated with Anticentromere Antibody.

13. A. Acute inflammation

Acute pancreatitis

14. C. D. Parvovirus B19

Two of the sources say that the answer is D. Parvovirus B 19 (maybe because it has to do with sickle cell anemia hence the hemoglobin & hematocrit is low but then wouldn’t you see sickle cell shape instead). Plus, parvovirus affect RBC precursors (reticulocytes), so, isn’t the ret ct kinda normal (since this is the case, you know that the bone marrow is working and it is compensation. E. Pneumocystis jiroveci (formerly P.carinii) is usually seen in adults.

AIDS
Parvovirus B19 is a cause of chronic anemia in individuals who have AIDS. It is frequently overlooked. Treatment with erythropoetin or intravenous immunoglobulin have been helpful in some patients. The parvovirus infection may trigger an inflammatory reaction in AIDS patients who have just begun antiretroviral therapy.[14].

http://en.wikipedia.org/wiki/Parvovirus_B19

15. G. Parathorone-related protein

When associated with the lung, it often causes ectopic production of parathyroid hormone-related protein (PTHrP), resulting in hypercalcemia.

Squamous-cell carcinoma of the lung is more common in men than in women. It is closely correlated with a history of tobacco smoking, more so than most other types of lung carcinoma. It most often arises centrally in larger bronchi, and while it often metastasizes to locoregional lymph nodes (particularly the hilar nodes) early in its course, it generally disseminates outside the thorax somewhat later than other major types. Large tumors may undergo central necrosis, resulting in cavitation. A squamous-cell carcinoma is often preceded for years by squamous-cell metaplasia or dysplasia in the respiratory epithelium of the bronchi, which later transforms to carcinoma in situ. In carcinoma in situ, atypical cells may be identified by cytologic smear test of sputum, bronchoalveolar lavage or samples from endobronchial brushings. However, squamous-cell carcinoma in situ is asymptomatic and undetectable on X-ray radiographs. Eventually, it becomes symptomatic, usually when the tumor mass begins to obstruct the lumen of a major bronchus, often producing distal atelectasis and infection. Simultaneously, the lesion invades into the surrounding pulmonary substance. On histopathology, these tumors range from well-differentiated, showing keratin pearls and cell junctions, to anaplastic with only minimal residual squamous-cell features.
http://en.wikipedia.org/wiki/Squamous-cell_carcinoma

16. A. Alkaline phosphatase activity

Paget's disease may be diagnosed using one or more of the following tests:

Pagetic bone has a characteristic appearance on X-rays. A skeletal survey is therefore indicated.

http://upload.wikimedia.org/wikipedi...gets_skull.jpg

An elevated level of alkaline phosphatase in the blood in combination with normal calcium, phosphate, and aminotransferase levels in an elderly patient are suggestive of Paget's disease.
Bone scans are useful in determining the extent and activity of the condition. If a bone scan suggests Paget's disease, the affected bone(s) should be X-rayed to confirm the diagnosis

The pathogenesis of Paget's disease is described in 3 stages, which are:
i. Osteoclastic activity
ii. Mixed osteoclastic-osteoblastic activity
iii. Exhaustive (burnt out) stage


Initially, there is a marked increase in the rate of bone resorption at localized areas caused by large and numerous osteoclasts. These localized areas of osteolysis are seen radiologically as an advancing lytic wedge in long bones or osteoporosis circumscripta in the skull. The osteolysis is followed by a compensatory increase in bone formation induced by osteoblasts recruited to the area. This is associated with accelerated deposition of lamellar bone in a disorganized fashion. This intense cellular activity produces a chaotic picture of trabecular bone ("mosaic" pattern), rather than the normal linear lamellar pattern. The resorbed bone is replaced and the marrow spaces are filled by an excess of fibrous connective tissue with a marked increase in blood vessels, causing the bone to become hypervascular. The bone hypercellularity may then diminish, leaving a dense "pagetic bone," also known as burned-out Paget's disease.

17. A. Discuss comfort care with the patient’s wife

all choices except A are artificial procedures that prolong his life.

18. D. Schistocytes

Normal lactate dehydrogenase is 25-90 U/L…this patient has 1000 U/L..definitely TTP

TTP: Thrombotic Thrombocytopenia Purpura: is a rare disorder of the blood-coagulation system, causing extensive microscopic thromboses to form in small blood vessels throughout the body (thrombotic microangiopathy). Most cases of TTP arise from inhibition of the enzyme ADAMTS13, a metalloprotease responsible for cleaving large multimers of von Willebrand factor (vWF) into smaller units. A rarer form of TTP, called Upshaw-Schülman syndrome, is genetically inherited as a dysfunction of ADAMTS13. If large vWF multimers persist there is tendency for increased coagulation.

http://en.wikipedia.org/wiki/Thrombo...openic_purpura

TPP: FA page 349) Symptoms: pentada of neurologic and renal symptoms, fever, thrombocytopenia, and microangiopathic hemolytic anemia.
Lab: Schistocytes, increase LDH.

19. B. GM2-ganglioside

Tay sach disease: AR, Progresive neurodegeneration, developmental delay, cherry red spot on macula, lysosomal with onion skin , NO HEPATOMEGALY. Def. enzime: Hexosaminidase A; Accumulated substrate: G2 ganglioside. (FA page 111).

20. B. Smell

Olfatory CN I is the only CN without thalamic relay to cortex. Function: Smell ( FA 413)

21. F. Increased volume of distribution

22. D. Pneumothorax

Pneumothorax is defined as the presence of air or gas in the pleural cavity, that is, in the potential space between the visceral and parietal pleura of the lung. The result is collapse of the lung on the affected side. Air can enter the intrapleural space through a communication from the chest wall (ie, trauma) or through the lung parenchyma across the visceral pleura.

Primary spontaneous pneumothorax (PSP) occurs in people without underlying lung disease and in the absence of an inciting event . In other words, air is present in the intrapleural space without preceding trauma and without underlying clinical or radiologic evidence of lung disease.

Risks factors for primary spontaneous pneumothorax (PSP) include the following:

•Smoking
•Tall, thin stature in a healthy person
•Marfan syndrome
•Pregnancy
•Familial pneumothorax
Blebs and bullae (sometimes called emphysematouslike changes or ELCs) are related to the occurrence of primary spontaneous pneumothorax.


Secondary spontaneous pneumothorax (SSP) occurs in people with a wide variety of parenchymal lung diseases, that is, these individuals have underlying pulmonary structural pathology (see the image below). Air enters the pleural space via distended, damaged, or compromised alveoli. Patients may present with more serious clinical symptoms and sequelae due to comorbid conditions.

Diseases and conditions associated with secondary spontaneous pneumothorax include the following:

•Chronic obstructive lung disease (COPD) or emphysema: Increased pulmonary pressure due to coughing with a bronchial plug of mucus or phlegm bronchial plug may play a role.
•Asthma
•Human immunodeficiency virus/acquired immunodeficiency syndrome (HIV/AIDS) with PCP infection
•Necrotizing pneumonia
•Tuberculosis
•Sarcoidosis
•Cystic fibrosis
•Bronchogenic carcinoma or metastatic malignancy
•Idiopathic pulmonary fibrosis
•Inhalational and intravenous drug use (eg, marijuana, cocaine)[8]
•Interstitial lung diseases associated with connective tissue diseases
•Lymphangioleiomyomatosis
•Langerhans cell histiocytosis
•Severe acute respiratory syndrome (SARS): A reported 1.7% of SARS patients developed spontaneous pneumothorax.
•Thoracic endometriosis and catamenial pneumothorax
•Collagen vascular disease, including Marfan syndrome


23. C. Ganciclovir

Ganciclovir is an antiviral medication used to treat or prevent cytomegalovirus (CMV) infections
It is first phosphorylated to a deoxyguanosine triphosphate (dGTP) analogue. This competitively inhibits the incorporation of dGTP by viral DNA polymerase, resulting in the termination of elongation of viral DNA.

Adverse effects:
Ganciclovir is commonly associated with a range of serious haematological adverse effects. granulocytopenia, neutropenia, anaemia, thrombocytopenia, fever, nausea, vomiting, dyspepsia, diarrhoea, increased serum creatinine and blood urea concentrations

Toxicity:

Ganciclovir is considered a potential human carcinogen, teratogen, and mutagen. It is also considered likely to cause inhibition of spermatogenesis. Thus, it is used judiciously and handled as a cytotoxic drug in the clinical setting

24. E. Mitral regurgitation

Holosystolic murmur is best heard at the apex in the left lateral decubitus position....Mitral Regurgitation .

Murmur:

Blowing holosystolic murmur
Heard best at the apex
Radiation to the axilla and inferior edge of left scapula.
Possible associated findings:

S2: wide physiologic splitting
S3

http://depts.washington.edu/physdx/heart/tech.html

25. D. Rest (systolic < diastolic) vs. Moderate exercise (systolic < diastolic)
- the cardiac cycle where by coronary arteries deliver oxygen to the myocardium is during diastole........whether it is systolic or diastolic.....this is my assumption.
- no matter if the person is at rest or doing exercise, the coronary blood flow is always more during diastole. although the duration of flow is greatest during rest as oppose to exercise when the heart rate is faster and thus diastole is of less duration.

Coronary blood flow occurs mostly during diastole, because during systole the blood vessels within the myocardium are compressed. Increased heart rates, which reduce the time for diastole filling, can reduce the myocardial blood supply and cause ischemia.

Dynamic exercise increases coronary blood flow in proportion to the heart rate, with peak values during maximal exercise typically three to five times the resting level .

26. F. Surfactant

Severely premature infants may have underdeveloped lungs, because they are not yet producing their own surfactant. This can lead directly to respiratory distress syndrome, also called hyaline membrane disease, in the neonate.

To try to reduce the risk of this outcome, pregnant mothers with threatened premature delivery prior to 34 weeks are often administered at least one course of glucocorticoids, a steroid that crosses the placental barrier and stimulates the production of surfactant in the lungs of the fetus.

27. E. Increase B-hydroxybutyrate; increase osmality; increase anion gap

- Case of diabetic ketoacidosis...high glucose ...high ketones
- Betahydroxy butyrate and acetoacetate both increase.....
- Osmolarity =2 Serum Na+serum glucose /18+BUN/2.8 ...so if u increase glucose u increase
plasma osmolarity
- Anion Gap = Serum Na - (serum Chloride + Serum HCO3)...in the case of diabetic Ketoacidosis
- anions of acid (acetoacetate and beta hydroxybutyrate) replace HCO3 ...hence we only subtract Chloride from the Serum Na ...that makes the anion gap to increase....

n DKA
*beta-Hydroxybutyric acid is a ketone body....inc
*Due to loss of water......inc. serum osmolality.
*The anion gap is the difference in the measured cations and the measured anions in serum, plasma, or urine. The magnitude of this difference (i.e. "gap") in the serum is often calculated in medicine when attempting to identify the cause of metabolic acidosis.

only Na+, Cl− and HCO3− (+/- K) are used when calculating the anion gap... healthy adults is 8-12 mEq/L

( [Na+] ) − ( [Cl−]+[HCO3−] )

a useful mnemonic to remember the high anion gap is MUDPILES (methanol, uremia, diabetic ketoacidosis, propylene glycol, isoniazid, lactic acidosis, ethylene glycol, salicylates).


28. D. Pseudomonas aeruginosa

It is a Gram-negative, aerobic, rod-shaped bacterium with unipolar motility and oxidase positive

P. aeruginosa secretes a variety of pigments, including pyocyanin (blue-green),
Because it thrives on most surfaces, this bacterium is also found on and in medical equipment, including catheters, causing cross-infections in hospitals and clinics. It is implicated in hot-tub rash.

29. E. Mitral valve prolapse

Marfan syndrome can lead to mitral valve prolapse (MVP)

30. A. Increase hemoglobin F; increase Hemoglobin A2: hemoglobin A ratio; increase reticulocyte count
- Patient has beta thalassemia
o Normal adult hemoglobin is alpha 2, beta 2, and alpha 2, gamma 2
o Increase HbA2 (>3.5%)
• You compare the ratio of Adult 2 with Adult 1
• Adult 2 is normal, hence, adult 2 has a higher normal adult hemoglobin than Adult 1
o Both major & minor = increase HbF (alpha 2; gamma 2)
• Adult 1 normally has alpha 2, beta 2
• Adult 2 normally has alpha 2, delta 2
• In beta thalassemia, you change beta 2 in adult 1 with HbF (alpha 2, gamma 2)
• So, now, the adult 1 has alpha 2, HbF…aka alpha 2, gamma 2
• Hence, you see an increase in HbF
o Reticulytes is normal/to increase because there is nothing wrong with the bone marrow so therefore, it doesn’t the reticulocytes.
o embryonic hemoglobin: 2z, 2e
o transition hemoglobin: 2z, 2y
o fetal hemoglobin: 2alpha, 2y
o adult hemoglobin HbA1: 2 alpha, 2 beta
o adult 2: 2 alpha, 2 delta

Beta thalasemia: prevalent in mediterranea population.
Defect: point mutation in splicing sites and promoter sequences
Beta thalasemia minor (heterozygote)
1. beta chain in unproduced
2. usually asyntomptomatic
3. Dx confirmed by increase HbA2 ( > 3.5%)
Beta thalasemia major: (Homozygote)
1. beta chain is absent- severe anemia requiring blood transfusion (2º hemochromatosis)
2. Marrow expansion ( crew cut on skull x-ray)- skeletal defromities, chipmunk facies
Both major and minor - increase Hb F (FA page 343).

31. G. B2 adrenergic agonist

Beta 2 adrenergic agonist: Bronchodilation (relax bronchial smooth mucles)

32. C. Thyroid-stimulating hormone

TSH: Thyroid-stimulating hormone (also known as TSH or thyrotropin) is a peptide hormone synthesized and secreted by thyrotrope cells in the anterior pituitary gland, which regulates the endocrine function of the thyroid gland. TSH is the 1st step in evaluation of thyroid function.

33. B. Adenocarcinoma of the endometrium

Adenocarcinoma of the endometrium:
Carcinoma endometrial is the Most common gynecologic malignancy. peak occurrence at 55-65 year of age. Clinically presents with vaginal bleeding. Typically proceeded by endometrial hyperplasia. Risk factors include prolonged use of estrogen without progestins, obesity, diabetes, hypertension, nulliparity and late menopause. Increase myometrial invasion, decrease prognosis. (FA page 487)

34. C. Globus pallidus

Parkinson disease
Surgery and deep brain stimulation
Placement of an electrode into the brain. The head is stabilized in a frame for stereotactic surgery. Treating motor symptoms with surgery was once a common practice, but since the discovery of levodopa, the number of operations declined. Studies in the past few decades have led to great improvements in surgical techniques, so that surgery is again being used in people with advanced PD for whom drug therapy is no longer sufficient.[35] Surgery for PD can be divided in two main groups: lesional and deep brain stimulation (DBS). Target areas for DBS or lesions include the thalamus, the globus pallidus or the subthalamic nucleus.[35] Deep brain stimulation (DBS) is the most commonly used surgical treatment. It involves the implantation of a medical device called a brain pacemaker, which sends electrical impulses to specific parts of the brain. DBS is recommended for people who have PD who suffer from motor fluctuations and tremor inadequately controlled by medication, or to those who are intolerant to medication, as long as they do not have severe neuropsychiatric problems.[29] Other, less common, surgical therapies involve the formation of lesions in specific subcortical areas (a technique known as pallidotomy in the case of the lesion being produced in the globus pallidus).[35]

35. A. Deep fibular (peroneal)

PED: peroneal; eversion; dorsiflexion

Deep Fibular nerve: Weakness inversion, Loss extension of the digits, loss dorsiflexion ( foot drop), sensory loss on antero lateral leg and dorso of the foot, first web space. (Kaplan anatomy page 295 and 295)

36. B. Placenta accrete

Placeta accreta: An invasion of the myometrium which does not penetrate the entire thickness of the muscle. This form of the condition accounts for around 75% of all cases.

Placenta perccreta: The worst form of the condition is when the placenta penetrates the entire myometrium to the uterine serosa (invades through entire uterine wall). This variant can lead to the placenta attaching to other organs such as the rectum or bladder[1

37. C. Ileum

Crohn Disease: Also known as regional enteritis, is an inflammatory disease of the intestines that may affect any part of the gastrointestinal tract from mouth to anus, causing a wide variety of symptoms. It primarily causes abdominal pain, diarrhea (which may be bloody if inflammation is at its worst), vomiting, or weight loss,[1][2][3] but may also cause complications outside the gastrointestinal tract such as skin rashes, arthritis, inflammation of the eye, tiredness, and lack of concentration.[1]

Crohn's disease is thought to be an autoimmune disease, in which the body's immune system attacks the gastrointestinal tract, causing inflammation; it is classified as a type of inflammatory bowel disease. There is evidence of a genetic link to Crohn's disease, putting individuals with siblings afflicted with the disease at higher risk.[4] It is thought to have a large environmental component as evidenced by a higher incidence in western industrialized nations compared to other parts of the world. Males and females are equally affected. Smokers are two times more likely to develop Crohn's disease than.

http://en.wikipedia.org/wiki/Crohn's_disease.
Gross morphology: transmural inflamation, Cobblestone mucosa, creeping fat, bowell wall thickning, (string sign on barium swallow x- ray) linear, ulcers, fissures, fistulas.
Microscopic morphology: Noncaseating granulomasand lymphoid

38. B. 0.19

positive predictive value Positive (PPV): TP/ (TP+FP)
PPV= 70/(70+300)= 0.18 in this case aprox. 0.19

39. C. Membranous nephropathy

Membranous Glomerulonephritis: LM -diffuse capillary and GBM thickening. EM " spike and dome" appearance with subepithelial deposits. IF - granular.

Caused by drugs ( penicillamine, Gold, NSAID). Most common cause of adult nephrotic syndrome.
The closely related terms membranous nephropathy[1] and membranous glomerulopathy[2] both refer to a similar constellation but without the assumption of inflammation.

Some patients may present as nephrotic syndrome with proteinuria, edema with or without renal failure. Others may be asymptomatic and may be picked up on screening or urinalysis as having proteinuria. A definitive diagnosis of membranous nephropathy requires a kidney biopsy.



40. A. Esctasy (3,4-methylenedioxymethamphetamine)

Intoxication for Amphetamine: Psychomotor agitation , impaired judgment, pupillary dilation, hypertension, tachycardia, euphoria, prolonged weakfulness sand attention, cardiac arrythmia, delusions, hallucinations, fever. (FA 448)

Amphetamine: Blocks of neurotransmiter uptake at the presynaptic nerve terminal

41. F. Tronchanteric bursa

- Trochanteric bursitis is characterized by painful inflammation of the bursa located just superficial to the greater trochanter of the femur. Patients typically complain of lateral hip pain, although the hip joint itself is not involved. The pain may radiate down the lateral aspect of the thigh.
- The term greater trochanteric pain syndrome (GTPS) is now being commonly substituted for trochanteric bursitis, because the inflammatory etiology of the pain is being refuted by current research, using ultrasonographic, magnetic resonance imaging (MRI) – based, and histologic evidence.
- Flexion or anteversion (140°): iliopsoas (with psoas major from vertebral column); tensor fascia latae, pectineus, adductor longus, adductor brevis, and gracilis. Thigh muscles acting as hip flexors: rectus femoris and sartorius.

42. E. X-linked recessive

Duchenne muscular dystrophy (DMD) is a recessive X-linked. The disorder is caused by a mutation in the dystrophin gene, located in humans on the X chromosome (Xp21). The dystrophin gene codes for the protein dystrophin, an important structural component within muscle tissue.

43. C. Medial collateral ligament

Medial collateral ligament" known as the tibial collateral ligament too.MCL strains and tears are fairly common in American football. Mostly the center and the guards are ones who get this injury, due to the grip trend on their cleats.

An MCL injury can be very painful and is caused by a valgus stress to a slightly bent knee, often when landing, bending or on high impact. Depending on the grade of the injury, the lowest grade (grade 1) can take between 2 and 10 weeks for the injury to fully heal. Recovery times for grades 2 and 3 are difficult to predict because of the amount of damage done can take weeks to several months. It is difficult to apply pressure on the injured leg for at least a few days.

44. A. They attributed the difference in success rates to chance alone

In order for it to be stagistical significance, you need the P value to be 0.05 aka 95%

But since the P value here is 0.3 aka 70%..it is only due to chance.

The P value for a study should be less than 0.05.

This value means that when we perform a study, the 95% of the time the observations are rite & 5 % of the time the observation are due to chance alone.

In this question the value of P is 0.3 which means that the probability that these observations are due to chance alone is 30%, which is not a statistically acceptable number.

45. E. St. John’s wort

St John's wort has been shown to cause multiple drug interactions through induction of the cytochrome P450 enzyme CYP3A4, but also CYP2C9. This results in the increased metabolism of those drugs, resulting in decreased concentration and clinical effect.
Examples of drugs causing clinically-significant interactions with St John's wort
Class Drugs
antiretrovirals non-nucleoside reverse transcriptase inhibitors, protease inhibitors
benzodiazepines alprazolam, midazolam
hormonal contraception combined oral contraceptives
immunosuppressants calcineurin inhibitors, ciclosporin, tacrolimus
others, digoxin, methadone, omeprazole, phenobarbitol, theophylline, warfarin, levodopa, suboxone, Irinotecan

46. D. Increased osmolarity in the tubular lumen (urine)
o the boy has DM type 1
o in type 1 you have high glucose, no insulin
o high glucose will reabsorb all of the water into the cells, this pull water away from the tubule (urine) and you get hypertonic urine

http://en.wikipedia.org/wiki/Diabetic_ketoacidosis

Osmotic diuresis is increased urination caused by the presence of certain substances in the small tubes of the kidneys.[1] The excretion occurs when substances such as glucose enter the kidney tubules and cannot be reabsorbed (due to a pathological state or the normal nature of the substance). The substances cause an increase in the osmotic pressure within the tubule, causing retention of water within the lumen, and thus reduces the reabsorption of water, increasing urine output (ie. diuresis). The same effect can be seen in therapeutics such as mannitol, which is used to increase urine output and decrease extracellular fluid volume.
Substances in the circulation can also increase the amount of circulating fluid by increasing the osmolarity of the blood. This has the effect of pulling water from the interstitial space, making more water available in the blood and causing the kidney to compensate by removing it as urine. In hypotension, often colloids are used intravenously to increase circulating volume in themselves, but as they exert a certain amount of osmotic pressure, water is therefore also moved, further increasing circulating volume. As blood pressure increases, the kidney removes the excess fluid as urine.
Sodium, chloride, potassium are excreted in Osmotic diuresis, originating from Diabetes Mellitus (DM). Osmotic diuresis results in dehydration from polyuria and the classic polydipsia (excessive thirst) associated with DM.
http://en.wikipedia.org/wiki/Osmotic_diuresis

47. A. 312
- CPM ...stands for count per minute ..which is a measure of radioactivity. It is the number of
atoms in a given quantity of radioactive material that are detected to have decayed in one
minute.
- Mixed Lymphocyte Reaction... a test used to check class II compatibilty testing ...in this test
lymphocytes from one individual being tested(donor ) are irradiated so that they cant proliferate..
but will act as a stimulator cells for the presentation of MHC antigens ...the other individual
cells (Recipient) are added to the culture ,and uptake of tritiated thymidine is used as an
indicator of cell proliferation....if the MHC class II antigens are different ,proliferation will
occur ..if they are the same, no proliferation will occurr....
- Proliferation is directly proportional to CPM
- high CPM .....high proliferation....MHC II different ...not compatible
- low CPM ...less proliferation...MHC II similar...less risk of rejection....compatible

MLR lymphocytes from the donor and recipient are mixed and allowed to react. If they are compatible there will not be stimulation and the lymphocyte may not proliferate, some lymphocytes will degenerate and the count will reduce, if they are not compatible the donor lymphocte will be stimulated and will start to proliferate with a increased count. You can see the only count that is smaller thean the host is 312.

if they are not compatible and the lymphocytes are activated and start proliferating, the donor lymphocytes will be outnumbered... the point is that you don't want the donor lymphocytes to proliferate at a higher rate than the guy's own...

http://books.google.com/books?id=EJX......ion&f=false

In this test, "stimulator" lymphocytes from a potential donor are first killed by irradiation and then mixed with live "responder" lymphocytes from the recipient; the mixture is incubated in cell culture to permit DNA synthesis, which is measured by incorporation of tritiated thymidine. The greater the amount of DNA synthesis in the responder cells, the more foreign are the class II MHC proteins of the donor cells. A large amount of DNA synthesis indicates an unsatisfactory "match"; i.e., donor and recipient class II (HLA-D) MHC proteins are not similar, and the graft is likely to be rejected. The best donor is, therefore, the person whose cells stimulated the incorporation of the least amount

48. B. Acidification causing increased ammonium ion excretion

Ammonium is basic, hence, to excrete it, you need to acidifiy it.

Lactulose inhibits bacterial ammonia production by acidifying the content of the bowel. It promotes growth of colonic flora. The growing biomass uses ammonia and nitrogen from amino acids to synthesise bacterial protein, which in turn inhibits protein degradation to NH3. Lactulose leads to less ammonia by inhibiting bacterial urea degradation and reduces colonic transit time, thus reducing the time available for ammonia production and expediting ammonia elimination.

49. D. Metaplasia of the esophageal epithelium
This is a case of GERD...with esophagitis for the last 8 months...
Gastroesophageal reflux disease (GERD) occurs when the amount of gastric juice that
refluxes into the esophagus exceeds the normal limit, causing symptoms with or without
associated esophageal mucosal injury (ie, esophagitis).
Pathogenesis of GERD...Transient relaxation of LES and Ineffective esophageal clearance of
reflux material (bile acid and gastric juice)...hence the amount of acid that is secreted by the
stomach doesnt have any significant effect ...also whether there is H pylori or not has no
significance ...as well as whether the stomach is atrophic or not ...

Hence I go for metaplasia of the esophageal epithelium (given the 8 month history )

Barrett's esophagus is a condition in which the normal squamous epithelium of the esophagus has been replaced by an abnormal red columnar epithelium called specialized intestinal metaplasia. Specialized intestinal metaplasia is red, like normal stomach tissue, but does not look like stomach tissue under the microscope.

50. E. urolithiasis

- acidic, low protein in the fluid meaning that the (normal protein is 1.02); blood 4+ (lots of hemolysis…so think RBC cast); glucose is negative is it is not bacteria bc bacteria takes up glucose; bilirubin is negative so it is not the liver problem; leukocyte esterase negative so it can’t be E. Coli;
o B. Nodular prostatic hyperplasia is not the answer because he is too you and he doesn’t alkaline phosphtase increase
o C. RCC is not it because RCC is chronic…this guy has acute
o D. Schistomoasis…is a worm..so you should see a present of eosophil…and plus this patient glucose is negative. F

Urolithiasis is the condition where urinary calculi are formed in the urinary tract.

Most common kidney stons...Calcium Oxalate,Calcium phosphate,or both...Radiopaque
Oxalate crystal..result fromEthylen glycol
Secound most common....Ammonium Magnesium phosphate..Struvite....caused by infecction with Urease-positive bugs.......can form staghorn calculi

Uric acid....associated with hyperuricemia........readiolucent

Cysteine...secondary to Cystinuria..Hexogonal shape.........faintly radiopaque...treat with alkalization

In some cases, kidney stones pass out of the body without producing any symptoms. Most kidney stones, however, do cause some symptoms. The most common symptom from kidney stones is pain. The pain from kidney stones is a result of the stone getting stuck on its way out.

If fever and chills accompany any of these symptoms, an infection may be present and medical attention is needed sooner rather than late.

Laboratory Testing:
Laboratory testing includes urinalysis to detect the presence of blood (hematuria) and bacteria (bacteriuria) in the urine.
Other tests include blood tests for creatinine (to evaluate kidney function), BUN and electrolytes to detect dehydration, calcium to detect hyperparathyroidism, and a complete blood count to detect infection.

X-rays: A standard x-ray of the kidney, ureter, and bladder, may be adequate as a first step for identifying many stones since most are visible on x-ray.

Ultrasound: This test uses high frequency sound waves to produce pictures. Ultrasounds can detect a dilated kidney and ureter caused by a stone lodged in the ureter. Ultrasound, however, cannot reliably detect all stones especially stones located outside the kidney. It is the preferred imaging method for kidney stone patients who are pregnant.

IVP (Intravenous Pyelogram): For an IVP, a special dye is injected into the patient's veins. The dye collects in the urinary system and produces a white shadow when an x-ray is taken. The dye allows to precisely locate the stone and to determine the condition of the kidneys and ureters. Most kidney stones can be precisely located using this procedure.

CT Scan (Computerized Tomography): This test uses a scanner and a computer to create images of the urinary system. A CT scan done to look for kidney stones does not use contrast material. It is the most common imaging test used today to evaluate a possible kidney stone attack.
It is a fantastic explanation, I wonder if you have the explanation for the other blocks?

Many thanks,
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Can anyone answer the C psittaci question?

An investigator develops an indirect immunofluoresoent immunoassay for detecting C psittaci in respiratory secretions.

Polyclonal antisera and monoclonal antibody are generated against a single killed strain of C. psittaci.

An initial enzyme immunoassay with the immunogenic strain shows comparable results with the polyclonal antisera or the monoclonal antibody.

In a clinical setting, however, it is found that the polydonal antisera are substantially more sensitive than the monoclonal antibody for detecting C. psittaca‘ infection.

Which of the following best explains this difference in sensitivity?


A) The affinity of the monoclonal antibody for its complementary epitope is lower than that of the polyclonal antisera

B) The avidity of the monoclonal antibody for its complementary epitope is lower than that of the polyclonal antisera

C) The fluorescein isothiocyanate label does not bind as tightly to the monoclonal antibody as It does to the polyclonal antisera

D) The greater diversity of epitopes recognized by the polyclonal antisera permits identification of strains not recognized by the monoclonal antibody

E) The monoclonal antibody lacks portions of the Fc region critical for recognition by anti-lgG antibodies in this indirect assay
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