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Need NBME 7,11,12 - ajavaheri62
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06-30-2011, 07:55 AM
Hi guys,
I need NBME 7,11, 12 with answers,can anyone send it to me please? my email adress:ajavaheri62 Thanks
06-09-2012, 09:20 AM
hi, if someone sends them to you, could you forward them: ryhm@live.fr
thank you
06-14-2012, 04:15 PM
can somebody forward nbme form7 at asabaqureshi.
thanks in advance
06-14-2012, 07:16 PM
7.1
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 7.2 1-5 AABBE 6-10 CEBAE 11-15 DDDBA 16-20 DECED 21-25 BBDDB 26-30 ADEDC 31-35 DDEEE 36-40 EEDAA ....need explanation for #39, I thought it was E: decreased RBF 41-45 BDCDB 46-50 CDCBB .....need explanation for #48, no clue whatsoever 7.3 1-5 ACDEC 6-10 AEBDC 11-15 ACCBB 16-20 AEDBB 21-25 DBAAD 26-30 EBACA 31-35 ECBAD 36-40 DACAE 41-45 CABAB 46-50 DEDAE 7.4 1-5 AAAAA #3 is NOT D because this patient presents as nephrotic NOT nephritic!! 6-10 BEBDC 11-15 AABAE 16-20 CCFAA 21-25 EGBBA #24 is NOT major depressive disorder because patient does not display suicidal thoughts....this answer should be bipolar, answer B 26-30 DDBCC 31-35 AECFC #34 count repeats for normal Q allele - it is 6 repeats so go onto graph, the risk is 0%; count repeats for expansion, it is total of 15 repeats so intersect it with the line and it corresponds with 60% risk 36-40 DCDDD 41-45 BBABB 46-50 CCADC
06-14-2012, 07:27 PM
NBME 11 NBME 11 NBME 11
http://www.usmleforum.com/showthread.php?tid=588232 BLOCK 1 1.FF since TB is a reportable disease 2.CC When blood sugar is low, glucagon signals the adipocytes to activate hormone-sensitive lipase, and to convert triglycerides into free fatty acids 3.EE Ninety percent of patients with gout develop excess urate stores due to an inability to excrete sufficient amounts of normally produced uric acid in the urine (underexcretion). The remaining patients either overconsume purines or produce excessive amounts of uric acid endogenously (overproduction). •In rare cases, overproduction of uric acid is primary, due to a genetic disorder. These disorders include hypoxanthine-guanine phosphoribosyltransferase deficiency (Lesch-Nyhan syndrome), glucose-6-phosphatase deficiency (von Gierke disease), fructose 1-phosphate aldolase deficiency, and PP-ribose-P synthetase variants. •Overproduction of uric acid may also occur in disorders that cause high cell turnover with release of purines, such as meat intake and seafood intake. These disorders include myeloproliferative and lymphoproliferative disorders, psoriasis, chemotherapy (tissue lysis), hemolytic anemias, pernicious anemia, ineffective erythropoiesis (as in B-12 deficiency), excessive exercise, and obesity. •Overproduction of uric acid can occur from overconsumption of foods high in purines. •Common causes of secondary gout due to underexcretion of uric acid include renal insufficiency, lead nephropathy (saturnine gout), starvation or dehydration, hypothyroidism, hyperparathyroidism, drugs (including loop and thiazide diuretics and cyclosporine A), low-dose aspirin, and chronic ethanol (especially beer and hard liquor) abuse. These disorders should be identified and corrected, if possible. •Comorbidities, including hypertension, diabetes, renal insufficiency, hypertriglyceridemia, hypercholesterolemia, diabetes, obesity, and early menopause, are associated with a higher incidence of gout. •Consumption of fructose-rich foods and beverages are associated with an increased risk of gout in both men and women Because of no clinical symptoms or history we should think about risk factors that can cause Gout... ....gender...Men more than women .......................age.....elderly more than younger 4.CC Gardenella vaginalis....gram variable rod...cause vaginosis white/gray vaginal discharge Whiff test...add KOH...fishy smell non painful anaerobe overgrowth of bacteria in vagina Clue cells or vaginal epithelial cell covered with bacteria treatment....Metronidazole 5.AA Check 1904 Q in UW 6.CC Lovastatin....-statins HMG-CoA reductase inhibitors...dec.LDL.. Bad cholestrol...mild effect on HDL and triglycerides...inc. mechanism of action.... 1.inhibit cholesterol precursor , mevalonate 2.synthesizing LDL receptors 7.CC 2-Naphthylamine is an aromatic amine. It is used to make azo dyes. It is a known human carcinogen. Aniline dyes...aromatic amines 2-Naphthylamine is found in cigarette smoke and suspected to contribute to the development of transitional cell carcinoma of urinary tract system (It is activated in the liver but quickly deactivated by conjugation to glucuronic acid. In the bladder, glucuronidase re-activates it by deconjugation, which leads to the development of bladder cancer.) 8.DD Presentation •Pin-point pupils, severe respiratory depression/cyanosis and coma. •BP may be low but is often surprisingly well maintained and with pentazocine overdose actually increases. •Although some opiates, e.g. dextropropoxyphene and pethidine, increase muscle tone and cause fits, in general opiates cause marked hypotonia. 9.CC Mesothelioma....It is usually caused by exposure to asbestos. Asbestosis...Ferruginous bodies...Asbestos bodies with prussian blue iron stain in the lung. 10.DD plasmid transfer between bacterias needs cell to cell contact through conjugation. And E coli is notorious for that. Bacterial transformation may be referred to as a stable genetic change brought about by the uptake of naked DNA (DNA without associated cells or proteins) and competence refers to the state of being able to take up exogenous DNA from the environment. Two forms of competence exist: natural and artificial. 11.CC Candida albicans....oral and esophageal thrush in immunocompromised...neonates,steroides,diabetes,AIDS and Vulvaginitis.....high PH diabetes,use of antibiotics Diaper rash and endocarditis in IV drug users, disseminated candidiasis to any organ,chronic mucocutaneous candidiasis Treatment....Nystatin for superficial infection( swish and swallow) Amphtericin B..for serious systemic infection 12.CC The palmar branch of the median nerve is a branch which arises at the lower part of the forearm. It pierces the palmar carpal ligament, and divides into a lateral and a medial branch; The lateral branch supplies the skin over the ball of the thumb, and communicates with the volar branch of the lateral antibrachial cutaneous nerve. The medial branch supplies the skin of the palm and communicates with the palmar cutaneous branch of the ulnar. Unlike most of the median nerve innervation of the hand, the palmar branch travels superficial to the Flexor retinaculum of the hand. Therefore, this portion of the median nerve usually remains functioning during carpal tunnel syndrome. 13.CC 2,3-Bisphosphoglycerate: It binds with greater affinity to deoxygenated hemoglobin (e.g. when the red cell is near respiring tissue) than it does to oxygenated hemoglobin 14.AA Acute coronary syndrome (ACS) is usually one of three diseases involving the coronary arteries: ST elevation myocardial infarction (30%), non ST elevation myocardial infarction (25%), or unstable angina (38%) The cardinal sign of decreased blood flow to the heart is chest pain experienced as tightness around the chest and radiating to the left arm and the left angle of the jaw. This may be associated with diaphoresis (sweating), nausea and vomiting, as well as shortness of breath. In many cases, the sensation is "atypical", with pain experienced in different ways or even being completely absent (which is more likely in female patients and those with diabetes). Some may report palpitations, anxiety or a sense of impending doom and a feeling of being acutely ill. 15.AA Albuterol....Beta2 agonist...relaxes bronchial smooth muscle ....used during acute exacerbation ...............................................Gs...................................................................... Beta1,Beta2,D1,H2,V2 receptors..........Adenyl cyclase.....ATP..> inc.cAMP.....>inc.Protein Kinase A 16 AA 17 CC CMV has a unique method of escaping immune response it dec. the expression of MHC 1 and also expresses a decoy molecule. The normal for the MHC 1 molecule is that its made in the RER and then transported to the Cell membrane. If it get translocated to the cytosol, its likely to be degraded. Ref Kaplan Immuno Chap 8[pg 99] viral strategies for evasion of the CMI response 18.GG Pupillary reflex: The oculomotor nerve also controls the constriction of the pupils and thickening of the lens of the eye. This can be tested in two main ways. By moving a finger toward a person's face to induce accommodation, as well as his going cross-eyed, his pupils should constrict. Shining a light into one eye should result in equal constriction of the other eye. The neurons in the optic nerve decussate in the optic chiasm with some crossing to the contralateral optic nerve tract. This is the basis of the "swinging-flashlight test". 19 DD 20.CC Kernicterus is damage to the brain centers of infants caused by increased levels of unconjugated bilirubin 21.BB http://www.helpguide.org/elder/lewy_body_disease.htm http://www.alz.org/alzheimers_disease_de...bodies.asp Lewy bodies are abnormal aggregates of protein that develop inside nerve cells in Parkinson's disease (PD) and Alzheimer's disease (AD) and some other disorders. They are identified under the microscope when histology is performed on the brain. Parkinson's disease....degenerative disorder of CNS associated with lewy bodies and depigmentation of the substantia nigra,loss of dopaminergic neurons rare cases have been linked with ilicit street drug...heroin 22.EE Hypothyroidism is a condition leading to the deficiency in the production of thyroid hormone. Subclinical hypothyroidism is a state of normal thyroid hormone levels, thyroxine (T4) and triiodothyronine (T3), with mild elevation of thyrotropin, thyroid-stimulating hormone (TSH). With higher TSH levels and low free T4 levels, symptoms become more readily apparent in clinical (or overt) hypothyroidism. Early.... Poor muscle tone (muscle hypotonia) Fatigue Any form of menstrual irregularity and fertility problems Hyperprolactinemia and galactorrhea Elevated serum cholesterol Cold intolerance, increased sensitivity to cold Constipation Rapid thoughts Depression Muscle cramps and joint pain Thin, brittle fingernails Coarse hair Paleness Decreased sweating Dry, itchy skin Weight gain and water retention Bradycardia Late...... Goiter Slow speech and a hoarse, breaking voice – deepening of the voice can also be noticed, ma. Dry puffy skin, especially on the face Thinning of the outer third of the eyebrows Abnormal menstrual cycles Low basal body temperature Thyroid-Related Depression Uncommon......... Impaired memory Impaired cognitive function (brain fog) and inattentiveness. A slow heart rate with ECG changes including low voltage signals. Diminished cardiac output and decreased contractility Reactive (or post-prandial) hypoglycemia Sluggish reflexes Hair loss Anemia caused by impaired haemoglobin synthesis (decreased EPO levels), impaired intestinal iron and folate absorption or B12 deficiency Difficulty swallowing Shortness of breath with a shallow and slow respiratory pattern Increased need for sleep Irritability and mood instability Yellowing of the skin due to impaired conversion of beta-carotene to vitamin A Impaired renal function with decreased glomerular filtration rate Acute psychosis (myxedema madness) (a rare presentation of hypothyroidism) Decreased libido in men due to impairment of testicular testosterone synthesis Decreased sense of taste and smell (anosmia) Puffy face, hands and feet (late, less common symptoms) Gynecomastia Deafness 23.DD The palmaris longus is seen as a small tendon between the flexor carpi radialis and the flexor carpi ulnaris, although it is not always present. The muscle is absent in about 14 percent of the population Absence of palmaris does not have any known effect on grip strength 24.AA Pertusis toxin inhibits Gi, so causes increase in cAMP -Lymphocytosis promotion -Hypoglycemia due to release of insulin. Pertusis Toxin interferes with the early chemokine production and the inhibition of the neutrophil chemotaxis. Chemokines are signaling molecules produced by infected cells and attract neutrophils and macrophages. 25.EE Barrier dysfunction is present in patients with Crohn's disease as well as some of their healthy first degree relatives. It has therefore been suggested that increased tight junction permeability (reduced barrier function) is a risk factor for development of Crohn's disease. 26.AA Narrowing renal artery inc. Renin-Angiotensin-Aldosteron system....... 27.DD irreversible cell injury Plasma membrane damage lysosomal rupture Calcium ion influx....oxidative phosphorylation, nuclear pycnosis,karyolysis, Mitochondrial pemeability....vacualization and phospholipid-containing amorphous density 28.BB The addictive potential of codeine encouraged the marketing of dextromethorphan in a variety of cough and cold preparations. Although dextromethorphan is chemically derived from the opiates, it has no analgesic or addictive properties. The cough suppression potency of dextromethorphan in adults is nearly equal to that of codeine.2 The drug, like codeine, acts on the central nervous system to elevate the threshold for coughing. 29.EE Bone marrow transplant has been shown to induce tolerance following organ transplant. 30.AA The patient is too tall and thin with scoliosis.....Marfan's....cystic medial necrosis Aortic dissection..present with tearing chest pain radiating to the back.... CXR.. mediastinal widening 31.DD adult cell type is replaced by another...often secondary to irritation/or environmental exposure Barrett's esophagous....Glandular metaplasia...replacement of non keratinized squamous epithelium with intestinal/columnar epithelium in the distal esophagous due to chronic acid reflux. .GERD 32. E Brain Lymphoma (PCNSL), also known as micro glioma and primary brain lymphoma, is a primary intracranial tumor appearing mostly in patients with severe immunosuppression (typically patients with AIDS). PCNSLs represent around 20% of all cases of lymphomas in HIV infections (other types are Burkitt's lymphomas and immunoblastic lymphomas). is highly associated with Epstein-Barr virus (EBV) infection (> 90%) in immunodeficient patients (such as those with AIDS and those iatrogenically immunosuppressed), and does not have a predilection for any particular age group. usually presents with seizure, headache, cranial nerve findings, altered mental status, or other focal neurological deficits typical of a mass effect Systemic symptoms may include fever, night sweats, or weight loss. Other symptoms include • diplopia • dysphagia • vertigo • monocular vision loss • progressive dementia or stupor in patients with a non focal neurologic exam and minimal abnormalities on MRI (more common in AIDS patients) • facial hypoesthesia The definitive diagnosis is arrived at from tissue, i.e. a biopsy, by a pathologist. MRI or contrast enhanced CT classically shows multiple ring-enhancing lesions in the deep white matter. The major differential diagnosis (based on imaging) is cerebral toxoplasmosis, which is also prevalent in AIDS patients and also presents with a ring-enhanced lesion, although toxoplasmosis generally presents with more lesions and the contrast enhancement is typically more pronounced. imaging techniques cannot distinguish the two conditions with certainty, and cannot exclude other diagnoses. Thus, patients undergo a brain biopsy 33. C The patients treated with the new drug the duration of the outbreak was 1 week, instead that the duration of the patients treated with the placebo was 2 week. It mean that the prevalence in the group treated with the new drug ↓ by half. 34. D Hemorrhoids -- vascular structures in the anal canal which help with stool control. They become pathological or piles when swollen or inflamed. In their physiological state they act as a cushion composed of arterio-venous channels and connective tissue that aid the passage of stool. The symptoms of pathological hemorrhoids depend on the type present. Internal hemorrhoids usually present with painless rectal bleeding while external hemorrhoids present with pain in the area of the anus. Recommended treatment consists of increasing fiber intake, oral fluids to maintain hydration, NSAID analgesics, sitz baths, and rest. Surgery is reserved for those who fail to improve following these measures. 35. B Metoclopramide -- antiemetic and gastroprokinetic agent. Thus it is primarily used to treat nausea and vomiting, and to facilitate gastric emptying in patients with gastroparesis. It is also a primary treatment for migraine headaches. 36. E NNRTI: Nevirapine, Efavirenz, Delavirdine: Mechanism of action: Preferentially inhibit reverse transcriptase of HIV, prevent incorporation of DNA copy of viral genome into the host DNA. ( FA 2010 page 195) 37. C Congenital hearing loss --hearing loss present at birth. Can be hereditary or due to other factors present either in utero (prenatal) or at the time of birth. Treatment: A child with a congenital hearing loss should begin receiving treatment before 6 months of age. Studies suggest that children treated this early are usually able to develop communication skills (using spoken or sign language) that are as good as those of hearing peers. In the United States of America, because of a Federal law (the Individuals with Disabilities Education Act), children with a hearing loss between birth and 3 years of age have the right to receive interdisciplinary assessment and early intervention services at little or no cost. After age 3, early intervention and special education programs are provided through the public school system. 38. B Acidosis Respiratory: ↓ PO2,↓ PH , ↑CO2 39. A The formation of granulation tissue in an open wound allows the re epithelialization phase to take place, as epithelial cells migrate across the new tissue to form a barrier between the wound and the environment.Basal keratinocytes from the wound edges and dermal appendages such as hair follicles, sweat glands and sebacious (oil) glands are the main cells responsible for the epithelialization phase of wound healing. They advance in a sheet across the wound site and proliferate at its edges, ceasing movement when they meet in the middle. Keratinocytes migrate without first proliferating.Migration can begin as early as a few hours after wounding. However, epithelial cells require viable tissue to migrate across, so if the wound is deep it must first be filled with granulation tissue.Thus the time of onset of migration is variable and may occur about one day after wounding.Cells on the wound margins proliferate on the second and third day post-wounding in order to provide more cells for migration. 40. D Ropinirole -- non-ergoline dopamine agonist. -- acts as a D2, D3, and D4 dopamine receptor agonist with highest affinity for D3. It is weakly active at the 5-HT2, and α2 receptors and is said to have virtually no affinity for the 5-HT1, benzodiazepine, GABA, muscarinic, α1, and β-adrenoreceptors. Ropinirole is metabolized primarily by cytochrome P450 CYP1A2, and at doses higher than clinical, is also metabolized by CYP3A4. At doses greater than 24 mg, CYP2D6 may be inhibited, although this has only been tested in vitro. 41. B The uterine artery usually arises from the anterior division of the internal iliac artery Uterine artery embolization (UAE) is a procedure where an interventional radiologist uses a catheter to deliver small particles that block the blood supply to the uterine body. If the procedure is done for the treatment of uterine fibroids it is also called uterine fibroid embolization (UFE). Under local anesthesia a catheter is introduced into the femoral artery at the groin and advanced under radiographic control into the uterine arterty. 42 EE CMI is an immune response that does not involve antibodies or complement but rather involves the activation of macrophages, natural killer cells (NK), antigen-specific cytotoxic T-lymphocytes, and the release of various cytokines in response to an antigen. immune system separated into two branches: humoral immunity, for which the protective function of immunization could be found in the humor (cell-free bodily fluid or serum) and cellular immunity, for which the protective function of immunization was associated with cells. CD4 cells or helper T cells provide protection against different pathogens. T cells cause death by apoptosis without using cytokines, therefore in cell mediated immunity cytokines are not always present. Cellular immunity protects the body by: 1. activating antigen-specific cytotoxic T-lymphocytes that are able to induce apoptosis in body cells displaying epitopes of foreign antigen on their surface, such as virus-infected cells, cells with intracellular bacteria, and cancer cells displaying tumor antigens; 2. activating macrophages and natural killer cells, enabling them to destroy pathogens; and 3. stimulating cells to secrete a variety of cytokines that influence the function of other cells involved in adaptive immune responses and innate immune responses. 43. C Schizophrenia: Periods of psychosis and disturbed behavior with a decline in functioning lasting > 6 months. Associated with ↑ dopaminergic activity, ↓dendritic branching. Marijuana use is a risk factor for schizophrenia in teens. It most commonly manifests as auditory hallucinations, paranoid or bizarre delusions, or disorganized speech and thinking, and it is accompanied by significant social or occupational dysfunction. 44. A Glibenclamide (INN), also known as glyburide (USAN), antidiabetic sulfonylureas, closely related to sulfa drugs. Mechanism of action: works by inhibiting ATP-sensitive potassium channels in pancreatic beta cells.--inhibition causes cell membrane depolarization, -- voltage-dependent calcium channels to open, -- an increase in intracellular calcium in the beta cell, which stimulates insulin release. 45. A Plasmodium vivax -- protozoal parasite ,a human pathogen. The most frequent and widely distributed cause of recurring (tertian) malaria one of the four species of malarial parasite that commonly infect humans. less virulent than Plasmodium falciparum, which is the deadliest of the four, and is seldom fatal. carried by the female Anopheles mosquito, Chloroquine remains the treatment of choice for vivax malaria 32 to 100% of patients will relapse following successful treatment of P. vivax infection if a radical cure (eradication of liver stages) is not given Eradication of the liver stages is achieved by giving primaquine, after checking the patients G6PD status to reduce the risk of haemolysis. However, in severe G6PD deficiency, primaquine is contraindicated and should not be used 46.EE vincristine.....M-phase specific alkaloides that bind to tubulin and block polymerization of microtubules...so that mitotic spindle can not form s/e...neurotoxicity....areflexia, peripheral neurities paralytic ileus Cyclophosphamide....alkylating agent..covalantly x-link DNA at guanine N-7, require bio activation by liver s/e...myelosuppression,hemorrhagic cystitis..can be prevented by mesna Doxorubicin: .....generate free radicals and noncovalantly intercalate in DNA s/e...Cardiotoxicity,myelosuppression and marked alopesia,toxic extravasation Rituximab: General side effects have included fever (49%), chills (32%), asthenia (16%), headache (14%), and abdominal pain (6%). 47.CC Perfusion pressure....the gradient between arterial blood pressure and venous pressure in a comparable location in the vascular tree....in this case the perfusion pressure is the pressure gradient between renal artery and renal vein...... relationship between flow(Q) ,Resistance®,and Perfusion pressure(P1-P2).... According to Poiseuille Equation P1-P2(Perfusion pressure)= R multiplied by Q..... P1= Renal artery pressure P2=Renal Vein pressure This patient has Hypotension Secondary to Severe Dehydration ....this causes the activation of the Sympathetic Nervous System ....and the RAA system ....both work independently even if the end result is the same ..... Sympathetic Nervous System causes Vasoconstriction of arteriolar beds including the renal arterioles ..... the sympathetic nervous system increases the resistance and decreases the flow (Q)....Therby decreasing perfusion pressure ( the difference between arterial presuure and venous pressure).... The RAA system ....AT II is a potent vasoconstrictor throughout the body ....including the afferent and efferent arterioles .....even if more on efferent ......When there is vasoconstriction of the afferent arterioles there will be a decrease in flow (Q)....which further decreases the perfusion pressure according to Poiseuille equation .... 48.AA immunologically compromised, esp those with HIV and low CD4 T cell counts, frequently show negative results from the PPD test. This is because the immune system needs to be functional to mount a response to the protein derivative injected under the skin. With the change from 10mm to 5 mm....there are more people can be identified with positive tuberculin test.... so incidence and prevalance will be higher The results of this test must be interpreted carefully. The person's medical risk factors determine at which increment (5 mm, 10 mm, or 15 mm) of induration the result is considered positive. A positive result indicates TB exposure. 5 mm or more is positive in HIV-positive person Recent contacts of TB case Persons with nodular or fibrotic changes on chest x-ray consistent with old healed TB Patients with organ transplants and other immunosuppressed patients 10 mm or more is positive in Recent arrivals (less than 5 years) from high-prevalence countries Injection drug users Residents and employees of high-risk congregate settings (e.g., prisons, nursing homes, hospitals, homeless shelters, etc.) Mycobacteriology lab personnel Persons with clinical conditions that place them at high risk (e.g., diabetes, prolonged corticosteroid therapy, leukemia, end-stage renal disease, chronic malabsorption syndromes, low body weight, etc.) Children less than 4 years of age, or children and adolescents exposed to adults in high-risk categories 49.CC The child has less opportunity to use her/his gross muscle for movement and development....so delayed gross motor development could be occurred 50.AA Hb electrophoresis---measures the different types of the oxygen-carrying protein (hemoglobin) in the blood. Many different types of hemoglobin (Hb) exist. The most common ones are HbA, HbA2, HbF, HbS, HbC, Hb H, and Hb M. Healthy adults only have significant levels of HbA and HbA2. Some people may also have small amounts of HbF (which is the main type of hemoglobin in an unborn baby's body). Certain diseases are associated with high HbF levels (when HbF is more than 2% of the total hemoglobin). HbS is an abnormal form of hemoglobin associated with sickle cell anemia. In people with this condition, the red blood cells sometimes have a crescent or sickle shape. The cells easily break down, or can block small blood vessels. HbC is an abnormal form of hemoglobin associated with hemolytic anemia. The symptoms are much milder than they are in sickle cell anemia. Other, less common, abnormal Hb molecules cause anemias. Normal Results In adults, these hemoglobin molecules make up the following percentages of total hemoglobin: •Hb A: 95% to 98% •Hb A2: 2% to 3% •Hb F: 0.8% to 2% •Hb S: 0% •Hb C: 0% In infants and children, these hemoglobin molecules make up the following percentages of total hemoglobin: •Hb F (newborn): 50% to 80% •Hb F (6 months): 8% •Hb F (over 6 months): 1% to 2% The presence of significant levels of abnormal hemoglobins may indicate: •Hemoglobin C disease •Rare hemoglobinopathy •Sickle cell anemia •Thalassemia BLOCK 2 1.CC Aspirin accetylates and irreversibaly inhibits cyclooxygenase..both coc1 and cox2 to prevent the conversion of arachidonic acid to thromoxane A2....inc. bleeding time ,no effect on PT and PTT. 2.FF Levofloxacin is a broad-spectrum antibiotic that is active against both Gram-positive and Gram-negative bacteria. It functions by inhibiting DNA gyrase, a type II topoisomerase, and topoisomerase iv which is an enzyme necessary to separate replicated DNA, thereby inhibiting cell division. 3.AA The deltoid is innervated by the axillary nerve. The axillary nerve originates from the ventral rami of the C5 and C6 cervical nerves, via the superior trunk, posterior division of the superior trunk, and the posterior cord of the brachial plexus. Axillary nerve lesion ***Sensory supply over deltoid ***Sensory loss small area over deltoid ***Area of pain across shoulder tip ***Motor deficit second 90° of shoulder abduction (deltoid) (teres minor cannot be evaluated) ***Causative lesions # neck of humerus, dislocated shoulder deep IM injection 4.BB Statistical significance= Is determined by P value.....and as see the p value is less than .05....hence for sure there is a difference between the two interventions (NOT BY CHANCE ALONE).....If the P Value is greater than .05 u can SAY the difference in the two interventions is due to CHANCE ALONE .....So A is out -Practical Importance means CLINICAL SIGNIFICANCE not Statistical....and clinical significance MUST ANSWER THE QUESTION ...how effective is the intervention or treatment in the CLINICAL SETTING....And the doctor made the CALL in this case not the researcher....And the way u measure CLINICAL SIGNIFICANCE IS by some of the following methods...EFFECT SIZE ,Number Needed to treat,and Preventive fraction..... -Already in the question u stated the magnitude of the difference was so small....How do they know ? They calculated NNT.... as u know NNT= 1/49%-45 %=1/4%=25.....Taking Program A as a control (as u know control groups can get placebo or as in this case STANDARD CARE).... -This means if the health official decided to change Program B as a STANDARD of CARE .....to treat HYPERCHOLSTEROLEMIA in 1 patient 25 should be INVOLVED ..... ---NNT=25 is not clinical significant.....hence choice B...... about the other choices.... Choice D....once you find the difference is STATISTICALLY SIGNIFICANT ...the sample size should be assumed LARGE and Enough...Only question sample size if the STUDY is not STATISTICALLY SIGNIFICANT....i.e When Calculated P Value is greater than .05..... Choice C....Many times the investigator will report the lowest COMPUTED P Value ....In general the smaller the p the BETTER...... And I remember a question on NBME 7 where the computed P value was greater than .05.....and the answer was ....Due to chance alone....but the scenario was almost the same as this question..... 5.BB HSV-1 is the more common cause of adult encephalitis. HSV-2 is the more common cause of newborn encephalitis. The encephalitis affects the temporal lobes of the brain in most cases 6.BB Pancreatic cancer is sometimes called a "silent killer" because early pancreatic cancer often does not cause symptoms,[4] and the later symptoms are usually nonspecific and varied.[4] Therefore, pancreatic cancer is often not diagnosed until it is advanced. Painless jaundice (yellow tint to whites of eyes and/or yellowish skin in serious cases, possibly in combination with darkened urine) when a cancer of the head of the pancreas (about 60% of cases) obstructs the common bile duct as it runs through the pancreas. This may also cause pale-colored stool and steatorrhea. The jaundice may be associated with itching as the salt from excess bile can cause skin irritation. 7-D Secretin is a hormone that controls the secretions into the duodenum, and also separately, water homeostasis throughout the body. It is produced in the S cells of the duodenum in the crypts of Lieberkühn.[1] Its effect is to regulate the pH of the duodenal contents via the control of gastric acid secretion and buffering with bicarbonate from the centroacinar cells of the pancreas as well as intercalated ducts. It is notable for being the first hormone to be identified. In humans, the secretin peptide is encoded by the SCT 8-E Opioids withdrawal produce, anxiety, insomnia, anorexia, sweating dilated pupils, piloerection (cold turkey), fever, rhinorrhea, nausea, stomach cramps, diarrhea (flulike symtoms) and yawning 9-D Raynaud's phenomenon is an exaggeration of vasomotor responses to cold or emotional stress. More specifically, it is a hyperactivation of the sympathetic system causing extreme vasoconstriction of the peripheral blood vessels, leading to tissue hypoxia Nefedipine vasodilate by releasing nitric oxide in smooth muscle, causing increased in cGMP and smooth muscle relaxation,. dilate veins more than arteries and dicreased the preload 10.C An exudate is any fluid that filters from the circulatory system into lesions or areas of inflammation. Its composition varies but generally includes water and the dissolved solutes of the main circulatory fluid such as sap or blood. In the case of blood: it will contain some or all plasma proteins, white blood cells, platelets and (in the case of local vascular damage) red blood cells. Transudate Exudate Main causes Increased hydrostatic pressure, Decreased colloid osmotic pressure Inflammation Appearance Clear Cloudy Specific gravity < 1.012 > 1.020 Protein content < 2 g/dL > 2.9 g/dL fluid protein serum protein < 0.5 > 0.5 Difference of albumin content with blood albumin > 1.2 g/dL < 1.2 g/dL fluid LDH upper limit for serum < 0.6 or < ⅔ > 0.6[5] or > ⅔ Cholesterol content < 45 mg/dL > 45 mg/dL[5 Exudate...An exudate is any fluid that filters from the circulatory system into lesions or areas of inflammation. it will contain some or all plasma proteins, white blood cells, platelets and (in the case of local vascular damage) red blood cells protein rich....specific gravity >1020 ***Types*** Purulent or suppurative exudate consists of plasma with both active and dead neutrophils, fibrinogen, and necrotic parenchymal cells. This kind of exudate is consistent with more severe infections, and is commonly referred to as pus. Fibrinous exudate is composed mainly of fibrinogen and fibrin. It is characteristic of rheumatic carditis, but is seen in all severe injuries such as strep throat and bacterial pneumonia. Fibrinous inflammation is often difficult to resolve due to the fact that blood vessels grow into the exudate and fill the space that was occupied by fibrin. Often, large amounts of antibiotics are necessary for resolution. Catarrhal exudate is seen in the nose and throat and is characterized by a high content of mucus. Serous exudate (sometimes classified as serous transudate) is usually seen in mild inflammation, with little protein content. Its consistency resembles that of serum, and can usually be seen in certain disease states like tuberculosis. (See below for difference between transudate and exudate) Malignant (or cancerous) pleural effusion is effusion where cancer cells are present. It is usually classified as exudate. Trasudate versus Exudate Hypocellular, Protein poor Specific gravity 11.DD Rigt heart failure....Jugular venous distantion and bilateral Ankle,sacral edema ..due to inc venous pressure 12.FF The dissociation curve shifts to the right when carbon dioxide or hydrogen ion concentration is increased. This facilitates increased oxygen dumping. This mechanism allows for the body to adapt the problem of supplying more oxygen to tissues that need it the most. The general equation for the Haldane Effect is: H+ + HbO2 ←→ H+Hb + O2 .It has asked the effect of shift of the O2 dissociation curve to the right due to an increase of H+... The answer should definitely be F,i.e., release of oxygen in tissue capillaries. That's what happens when pH falls and the curve shifts to the right.The unloading of O2 becomes easier in tissue capillaries.They have not mentioned anything regarding hypoxia in the question which u mentioned here. Rise in 2,3 BPG will also have the same effect, but the rise in 2,3 DPG is not solely due to rise in H+... 2,3-Bisphosphoglyceric acid ....interacts with deoxygenated hemoglobin beta subunits by decreasing their affinity for oxygen, so it allosterically promotes the release of the remaining oxygen molecules bound to the hemoglobin, thus enhancing the ability of RBCs to release oxygen near tissues that need it most. 13.CC A fat embolism is a type of embolism that is often (but not always) caused by physical trauma like fracture of long bones, soft tissue trauma and burns. Fat emboli occur in almost 90% of all patients with severe injuries to bones, although only 10% of these are symptomatic. The risk of fat embolism syndrome is thought to be reduced by early immobilization of fractures and especially by early operative correction. There is also some evidence that steroid prophylaxis of high-risk patients reduces the incidence. The mortality rate of fat-embolism syndrome is approximately 10-20%. The pathogenesis occurs due to both mechanical obstruction and biochemical injury. The microemboli cause pulmonary and cerebral microvasculature occlusion. It is aggravated by local platelet and erythrocyte aggregation. The release of free fatty acids from the fat globules causes local toxic injury to endothelium. The vascular damage is aggravated by platelet activation and recruitment of granulocytes. http://library.med.utah.edu/WebPath/HIST...IN011.html 14.AA http://www.google.com/imgres?imgurl=http...CEAQ9QEwAw 15.BB Coccidioidmycosis....mold in soil.....Southwestern US,California...causes pneumonia and meningitis(very rare). Can disseminate to bone and skin Culture...25degree...Hyphe with doubly reflective wall Biopsy Thick -wall spherules filled with endospores 16.AA In statistics, analysis of variance (ANOVA) is a collection of statistical models, and their associated procedures, in which the observed variance in a particular variable is partitioned into components attributable to different sources of variation. In its simplest form ANOVA provides a statistical test of whether or not the means of several groups are all equal, and therefore generalizes t-test to more than two groups. ANOVAs are helpful because they possess an advantage over a two-sample t-test. Doing multiple two-sample t-tests would result in an increased chance of committing a type I error. For this reason, ANOVAs are useful in comparing two, three or more means. 1-"Interval variable" (values from where we can drive their "Mean") e.g. measurements of B.P, Weight, Cholesterol levels etc 2-"Nominal variable" ( different categories or "GROUPS") e.g. *Gender ---is a Nominal that has Two Groups (Male and Female) *AGE-------is a Nominal that we can have either TWO groups (Elderly and Middle age) or THREE Groups(Elderly, Middle-age and Children) etc *Race------a Nominal that can have many groups Two groups (African Americans and Latino) Three groups(African Americans, Latino and Asian) and so forth e.g. *"GENDER"(Men and Women)....................................................(Single Nominal) *"GENDER"(Men and Women) n "RACE"(Caucasian and African)....(Two Nominals ) e.g we compare Blood Pressure measurements *INTERVAL variable ("MEANS" of B.P measurements) *NOMINAL variable ("GROUPS" ) so to compare MEANS of B.P. b/w two are more groups we do these tests t-Test: 1 Interval (Blood pressure Means) 1 Nominal with "ONLY TWO GROUPS" e.g. comparing the BP means b/w (Latinos) and (African Americans) *for a t-Test it will be a wrong statement to say e.g comparing B.P means b/w (Latinos), (African Americans) and (Asians)....*got 3 groups Now what's the difference B/W t-Test and ANOVA t-Test------>ONLY TWO Groups comparison ANOVA------------>TWO Groups or more than Two Groups comparison NOTE:these two will give u the Identical results if comparing "TWO Groups" t-Test................... 1 Interval and 1 Nominal with TWO Groups One-way ANOVA.....1 Interval and 1 Nominal with TWO Groups and for the above reason they rather use One-way ANOVA when more than two groups are there to be compared e.g as above comparing B.P means b/w (Latinos), (African Americans) and (Asians).......3 groups Two-way ANOVA: 1 Interval 2 Nominal e.g. Gender (Men and Women) *AND Race (Caucasians and African Americans) ---->we do these tests to see If there is a Difference b/w groups ? t-statistics (t-Test) and f-statistics(ANOVA) will be compared to get a p-value If p-value = 0.05 or less -----it is said to be "Statistically Significant' and we say that there is a Difference in these Groups. Chi-square: we compare b/w "TWO NOMINAL" (with ANY # of GROUPS) (Note; we are not using any Interval variable here , just the NOMINAL data) best example...."Testing Drug Efficacy" First Nominal........(New drug group) and (Placebo group) Second Nominal ...(Recovered group) and(Not recovered group) ***I think this is all u have to do is recognize what kind of data is presented , how many Nominals, How many groups and If Interval variable is used or not? 1 Interval and 1 Nominal (Two Groups).......................t-Test or One-way ANOVA 1 Interval and 1 Nominal (More than Two groups)........One-way ANOVA 1 Interval and *2 Nominal (many groups)....................Two-way ANOVA .....................*2 Nominal (any# of Groups).................Chi-square 17.DD Post-infectiousPost-infectious glomerulonephritis can occur after essentially any infection, but classically occurs after infection with Streptococcus pyogenes. It typically occurs 10–14 days after a skin or pharyngeal infection with this bacterium. Patients present with signs and symptoms of glomerulonephritis. Diagnosis is made based on these findings in an individual with a history of recent streptococcal infection. Streptococcal titers in the blood (antistreptolysin O titers) may support the diagnosis causes Nephritic syndrome...LM..glumeruli enlarged and hypercelullar Neutrophiles..Lumpy -Bumpy appereance Em...Subepithelial IC humps..IgM,IgG,C3 IF...granular resolve spontaneously 18.EE The thymus, is the principal organ responsible for the T cell's maturation. All T cells originate from haematopoietic stem cells in the bone marrow. Haematopoietic progenitors derived from haematopoietic stem cells populate the thymus and expand by cell division to generate a large population of immature thymocytes. The earliest thymocytes express neither CD4 nor CD8, and are therefore classed as double-negative (CD4-CD8-) cells. As they progress through their development they become double-positive thymocytes (CD4+CD8+), and finally mature to single-positive (CD4+CD8- or CD4-CD8+) thymocytes that are then released from the thymus to peripheral tissues. About 98% of thymocytes die during the development processes in the thymus by failing either positive selection or negative selection, whereas the other 2% survive and leave the thymus to become mature immunocompetent T cells. Positive selection "selects for" T-cells capable of interacting with MHC. Negative selection removes thymocytes that are capable of strongly binding with "self" peptides presented by MHC. 19. The answer should be B as they have asked which drug is to be given for 6 months after initiating therapy with heparin. Typically, before initiating warfarin therapy we start heparin to obtain immediate anticoagulation as warfarin takes time for it action. Immadiate anticoagulation for pulmonary embolism,stroke ,acute coronary syndrome Toxicity...bleeding Thrombocytopenis...HIT,osteoparosis,drug-drug interactions For rapid reversalof heparinization....PROTAMINE SULFATE ****Newer low molecular weight heparin...Enoxaparin act more on Xa have better bioavilibility without laboratory monitoring 20-E "Drug Y alone no effect" ( partial agonist are incapable of eliciting a maximal response and are less efecctive than the full agonist D-Noncompetitive Antagonist This is the case on the concept of "Spare Receptors" Assume ...100% receptor occupancy required by an Agonist to exert Maximum Effect (Emax) /Optimal effect. and now consider, if Emax is achieved with result *Efficacy of Drug X decreases *5 of the spare receptors are still Unoccupied Now if we raise the drug "X" dosage.....it will bind to the remaining unoccupied spare receptors and brings it Efficacy back to to the Emax. there for "No Change in Efficacy" , only "Potency decreases"(as needed higher dose of Drug X) ---------------------------------Graph on the Right-------------------------- But at "High Dose" of of NCA (Drug Y), it will bind to e.g all the 10 spare receptors---->result *Efficacy(Emax) of Drug X decreases *there are non of the spare receptors left unoccupied since there are no extra receptors left, even if we raise the Drug "X" dosage, it won't be able to increase it's Efficacy back to Emax. 21-E In treating hepatic encephalopathy, lactulose helps "draw out" ammonia (NH3) from the body.[5] Lactulose is metabolized in the colon by bacterial flora to short chain fatty acids including the production of the lactic acid and acetic acid. This partially dissociates, acidifying the colonic contents (increasing the H+ concentration in the gut).[6] This favors the formation of the nonabsorbable NH4+ from NH3, trapping NH3 in the colon and effectively reducing plasma NH3 concentrations. The effectiveness of lactulose in treating hepatic encephalopathy is somewhat controversial.[ Lactulose for hepatic encephalopathy generally requires oral dosage three or four times a day with diarrhea almost a certain side effect. 22-E A pheochromocytoma or phaeochromocytoma (PCC) is a neuroendocrine tumor of the medulla of the adrenal glands (originating in the chromaffin cells), or extra-adrenal chromaffin tissue that failed to involute after birth [1] and secretes excessive amounts of catecholamines, usually noradrenaline (norepinephrine), and adrenaline (epinephrine) to a lesser extent TO ADD; The signs and symptoms of a pheochromocytoma are those of sympathetic nervous system hyperactivity, including: Skin sensations Flank pain Elevated heart rate Elevated blood pressure, including paroxysmal (sporadic, episodic) high blood pressure, which sometimes can be more difficult to detect; another clue to the presence of pheochromocytoma is orthostatic hypotension (a fall in systolic blood pressure greater than 20 mmHg or a fall in diastolic blood pressure greater than 10 mmHg on making the patient stand) Palpitations Anxiety often resembling that of a panic attack Diaphoresis (excessive sweating) Headaches Pallor Weight loss Localized amyloid deposits found microscopically Elevated blood glucose level (due primarily to catecholamine stimulation of lipolysis (breakdown of stored fat) leading to high levels of free fatty acids and the subsequent inhibition of glucose uptake by muscle cells. Further, stimulation of beta-adrenergic receptors leads to glycogenolysis and gluconeogenesis and thus elevation of blood glucose levels). A pheochromocytoma can also cause resistant arterial hypertension. A pheochromocytoma can be fatal if it causes malignant hypertension, or severely high blood pressure. This hypertension is not well controlled with standard blood pressure medications 23.DD we need to cut 2lb=7000 cal (3500*2) 1 hr walk/d will cut 3500 cal In the meanwhile she is also getting 1800*7 calories=12600 in a week decrease intake for 500 cal /d * 7 days=3500 cal so 3500+3500=7000 It is a mathematic calculation... She is asked to loss 2 pounds weight weekly...each pounds=3500 cal and brisk walking consums 500cal per hour so........................................................... 2 pounds=7000cal she needs to loss 1000 cal per day......if she walked 2 hours per day....she could lose 1000 calories but between choices there is no 2 hours.so if she decreases 500 cal in her diet and gets 1 hour brisk walking then she will loss 1000 cal/day.......and 7000/week 24. C Systemic lupus erythematosus often abbreviated to SLE or lupus, is a systemic autoimmune disease (or autoimmune connective tissue disease) that can affect any part of the body. As occurs in other autoimmune diseases, the immune system attacks the body's cells and tissue, resulting in inflammation and tissue damage.[1] It is a Type III hypersensitivity reaction caused by antibody-immune complex formation. SLE most often harms the heart, joints, skin, lungs, blood vessels, liver, kidneys, and nervous system. The course of the disease is unpredictable, with periods of illness (called flares) alternating with remissions. In SLE, the body's immune system produces antibodies against itself, particularly against proteins in the cell nucleus. SLE is triggered by environmental factors that are unknown. "All the key components of the immune system are involved in the underlying mechanisms [of SLE]" according to Rahman, and SLE is the prototypical autoimmune disease. The immune system must have a balance (homeostasis) between being sensitive enough to protect against infection, and being too sensitive and attacking the body's own proteins (autoimmunity). From an evolutionary perspective, according to Crow, the population must have enough genetic diversity to protect itself against a wide range of possible infection; some genetic combinations result in autoimmunity. The likely environmental triggers include ultraviolet light, drugs, and viruses. These stimuli cause the destruction of cells and expose their DNA, histones, and other proteins, particularly parts of the cell nucleus. Because of genetic variations in different components of the immune system, in some people the immune system attacks these nuclear-related proteins and produces antibodies against them. In the end, these antibody complexes damage blood vessels in critical areas of the body, such as the glomeruli of the kidney; these antibody attacks are the cause of SLE. Researchers are now identifying the individual genes, the proteins they produce, and their role in the immune system. Each protein is a link on the autoimmune chain, and researchers are trying to find drugs to break each of those links. Renal Painless hematuria or proteinuria may often be the only presenting renal symptom. Acute or chronic renal impairment may develop with lupus nephritis, leading to acute or end-stage renal failure. Because of early recognition and management of SLE, end-stage renal failure occurs in less than 5% of cases. A histological hallmark of SLE is membranous glomerulonephritis with "wire loop" abnormalities.[16] This finding is due to immune complex deposition along the glomerular basement membrane, leading to a typical granular appearance in immunofluorescence testing. Lupus nephritis is an inflammation of the kidney caused by systemic lupus erythematosus (SLE), a disease of the immune system. Apart from the kidneys, SLE can also damage the skin, joints, nervous system and virtually any organ or system in the body. Histologically a wire-loop lesion will be present. The wire loop lesion is a glomerular capillary loop with subendothelial immune complex deposition that is circumferential around the loop. 25. E Kwashiorkor (pronounced /kwɑːʃiˈɔrkər/) is an acute form of childhood protein-energy malnutrition characterized by edema, irritability, anorexia, ulcerating dermatoses, and an enlarged liver with fatty infiltrates. The presence of edema caused by poor nutrition defines kwashiorkor.[1] Kwashiorkor was thought to be caused by insufficient protein consumption but with sufficient calorie intake, distinguishing it from marasmus. More recently, micronutrient and antioxidant deficiencies have come to be recognized as contributory. Cases in the developed world are rare. The defining sign of kwashiorkor in a malnourished child is pedal edema (swelling of the feet). Other signs include a distended abdomen, an enlarged liver with fatty infiltrates, thinning hair, loss of teeth, skin depigmentation and dermatitis. Children with kwashiorkor often develop irritability and anorexia. Marasmus is a form of severe protein-energy malnutrition characterized by energy deficiency. A child with marasmus looks emaciated. Body weight may be reduced to less than 80% of the average weight that corresponds to the height .[citation needed] Marasmus occurrence increases prior to age 1, whereas kwashiorkor occurrence increases after 18 months. It can be distinguished from kwashiorkor in that kwashiorkor is protein wasting with the presence of edema. The malnutrition associated with marasmus leads to extensive tissue and muscle wasting, as well as variable edema. Other common characteristics include dry skin, loose skin folds hanging over the glutei, axillae, etc. There is also drastic loss of adipose tissue from normal areas of fat deposits like buttocks and thighs. The afflicted are often fretful, irritable, and voraciously hungry. The word “marasmus” comes from a Greek word meaning starvation. Marasmus is generally known as the gradual wasting away of the body due to severe malnutrition or inadequate absorption of food. Marasmus is a form of severe protein deficiency and is one of the forms of protein-energy malfunction (PEM). It is a severe form of malnutrition caused by inadequate intake of proteins and calories. 26. C Primary polydipsia or psychogenic polydipsia is a special form of polydipsia.[1] It is usually associated with a patient's increasing fluid intake due to the sensation of having a dry mouth. When the term "psychogenic polydipsia" is used, it implies that the condition is caused by mental disorders. However, the dry mouth is often due to phenothiazine medications used in some mental disorders, rather than the underlying condition The patient drinks large amounts of water, which dilutes the extracellular fluid, decreasing its osmotic pressure. The body responds to this by decreasing the level of vasopressin (antidiuretic hormone), with a resultant increased production of urine (polyuria). This urine will have a low electrolyte concentration. Clinical presentation Patients have been known to seek fluids from any source possible. In extreme episodes, the patient's kidneys will be unable to deal with the fluid overload, and weight gain will be noted. Primary polydipsia can be life threatening as serum sodium is diluted to an extent that seizures and cardiac arrest can occur. 27. A Kawasaki disease: Acute, self-limiting necrotizing vasculitis in infants/ children. Association with Asia ethnicity. Fever, conjuntivitis, changes in lips/ oral mucosa (“strawberry tongue”), lymphadenitis, desquamative skin rash. May develop coronary aneurysms. 28. D In genetic medicine, a mosaic or mosaicism denotes the presence of two populations of cells with different genotypes in one individual who has developed from a single fertilized egg.[1] Mosaicism may result from a mutation during development which is propagated to only a subset of the adult cells. Somatic mosaicism Somatic mosaicism occurs when the somatic cells of the body are of more than one genotype. In the more common mosaics, different genotypes arise from only a single fertilized egg cell, due to mitotic errors at first cleavage. Another form of somatic mosaicism is chimerism, where two or more genotypes arise from the fusion of more than one fertilized zygote in the early stages of embryonal development. In rare cases, intersex conditions can be caused by mosaicism where some cells in the body have XX and others XY chromosomes.[2][3] The most common form of mosaicism found through prenatal diagnosis involves trisomies. Although most forms of trisomy are due to problems in meiosis and affect all cells of the organism, there are cases where the trisomy occurs in only a selection of the cells. This may be caused by a nondisjunction event in an early mitosis, resulting in a loss of a chromosome from some trisomic cells.[4] Generally this leads to a milder phenotype than in non-mosaic patients with the same disorder. An example of this is one of the milder forms of Klinefelter's syndrome, called 46/47 XY/XXY mosaic wherein some of the patient's cells contain XY chromosomes, and some contain XXY chromosomes. The 46/47 annotation indicates that the XY cells have the normal number of 46 total chromosomes, and the XXY cells have 47 total chromosomes. Around 30% of Turner's syndrome cases demonstrate mosaicism, while complete monosomy (45 XO) occurs in about 50–60% of cases. True mosaicism should not be mistaken for the phenomenon of X-inactivation, where all cells in an organism have the same genotype, but a different copy of the X chromosome is expressed in different cells, such as in calico cats. 29.C PaCO2=metabolic CO2 production/Va So if Ventilation increases to match up with CO2 production, PCO2 remains the same 30-F The classic triad for congenital rubella syndrome is: Sensorineural deafness (58% of patients) Eye abnormalities—especially cataract and microphthalmia (43% of patients) Congenital heart disease—especially patent ductus arteriosus (50% of patients) Other manifestations of CRS may include: Spleen, liver or bone marrow problems (some of which may disappear shortly after birth) Mental retardation Small head size (microcephaly) Eye defects Low birth weight Thrombocytopenic purpura (presents as a characteristic blueberry muffin rash) Hepatomegaly Micrognathia Children who have been exposed to rubella in the womb should also be watched closely as they age for any indication of the following: Developmental delay Autism spectrum disorders[1] Schizophrenia[2] Growth retardation Learning disabilities Diabetes Glaucoma Note:NO a congenital cytomegalovirus Generalized infection may occur in the infant, and can cause complications such as low birth weight, microcephaly, seizures, petechial rash similar to the "blueberry muffin" rash of congenital rubella syndrome, and moderate hepatosplenomegaly (with jaundice). 31. C Pityriasis or tiña versicolor caused by malassezia furfur. Degradation of lipids produces acids that damage melanocytes and cause hypopigmented patches. Occurs in hot humid weather. Yeast clusters & and short curved septate hyphae KOH scaping shows “spaghetti and meatballs”. Malassezia (formerly known as Pityrosporum) is a genus of fungi. Malassezia is naturally found on the skin surfaces of many animals, including humans. In occasional opportunistic infections, some species can cause hypopigmentation on the trunk and other locations in humans. T: Topical Miconazole, selenium sulfide. 32. A N. meningitidis: Gram neg. kidney bean shaped diploccoci, large capsule; latex particule agluttination ( or Counter immunoelectrophoresis ( CIE) to identify N. meningitidis capsular antigen in CSF. Reservorio: Human nasopharynx Transmision: Respiratory droplets; oropharyngeal colonization, spread to meninges via blood stream. Pathogenesis: Important virulent factor: Polysacharide capsule: antiphagocytic, antigenic, 5 common serogrups : B is not strongly immunogenic( sialid acid), B strain is most common strain in US. (Kaplan Microbiology book page 257) 33. D As a medical term, precocious puberty describes puberty occurring at an unusually early age. In most of these children, the process is normal in every respect except the unusually early age, and simply represents a variation of normal development. In a minority of children, the early development is triggered by a disease such as a tumor or injury of the brain. Even in instances where there is no disease, unusually early puberty can have adverse effects on social behavior and psychological development, can reduce adult height potential, and may shift some life-long health risks. Central precocious puberty can be treated by suppressing the pituitary hormones that induce sex steroid production. The term is used with several slightly different meanings that are usually apparent from the context. In its broadest sense, and often simplified as early puberty, "precocious puberty" sometimes refers to any physical sex hormone effect, due to any cause, occurring earlier than the usual age, especially when it is being considered as a medical problem. Stricter definitions of "precocity" may refer only to central puberty starting before a statistically specified age based on percentile in the population (e.g., 2.5 standard deviations below the population mean),[1] on expert recommendations of ages at which there is more than a negligible chance of discovering an abnormal cause, or based on opinion as to the age at which early puberty may have adverse effects. A common definition for medical purposes is onset before 8 years in girls or 9 years in boys. One possible treatment is with anastrozole. Histrelin acetate (Supprelin LA), Triptorelin or Leuprolide, any GnRH agonists, may also be used. GnRH agonists stimulate the pituitary to release Follicle Stimulating Hormone (FSH) and Luteinizing Hormone (LH). However, when used regularly, GnRH agonists cause a decreased release of FSH and LH. GnRH produced by the hypothalamus is pulsatile, allowing for a physiologic release of FSH and LH. 34-B Inhibitory synapses The neurotransmitter at inhibitory synapses hyperpolarizes the postsynaptic membrane. Example: gamma aminobutyric acid (GABA) at certain synapses in the brain. •The GABAA receptor is a ligand-gated chloride channel. Binding of GABA to the receptors increases the influx of chloride (Cl−  ions into the postsynaptic cell raising its membrane potential and thus inhibiting it.This is a fast response — taking only about 1 millisecond. •Binding of GABA to GABAB receptors activates an internal G protein and a "second messenger" that leads to the opening of nearby potassium (K+) channels. As you might expect, this is a slower response, taking as long as 1 second. In both cases, the resulting facilitated diffusion of ions (chloride IN; potassium OUT) increases the membrane potential (to as much as −80 mv). This increased membrane potential is called an inhibitory postsynaptic potential (IPSP) because it counteracts any excitatory signals that may arrive at that neuron. A hyperpolarized neuron appears to have an increased threshold. Actually, the threshold voltage (about −50 mv) has not changed. It is simply a question of whether the depolarization produced by excitatory synapses on the cell minus the hyperpolarizing effect of inhibitory synapses can reach this value or not. Mutation of the GABA, (no receptor) secundary to the mutation DECREASED THE influx of Cl- 35-F ADH is secreted in response to increased plasma osmolarity and dicreased blood volume, binds to receptors on principal cells, causing increased number of water channels and increased water reabsortion in the collecting tube. FA pag 396 The main effector organ for fluid homeostasis is the kidney. ADH acts by increasing water permeability in the collecting ducts and distal convoluted tubules, specifically it acts on proteins called aquaporins which open to allow water into the collecting duct cells. This increase in permeability allows for reabsorption of water into the bloodstream, thus concentrating the urine. Diabetes insipidus (DI) is a condition characterized by excessive thirst and excretion of large amounts of severely diluted urine, with reduction of fluid intake having no effect on the latter. There are several different types of DI, each with a different cause. The most common type in humans is central DI, caused by a deficiency of arginine vasopressin (AVP), also known as antidiuretic hormone (ADH). The second common type of DI is nephrogenic diabetes insipidus, which is caused by an insensitivity of the kidneys to ADH. It can also be an iatrogenic artifact of drug use. 36.CC Subdural hematoma....rupture of bridging vein crescent -shaped hemorrhage that crosses suture lines...cn not cross falx.tentorium venous bleeding with delayed onset ,seen in elderly,alcoholics,blunt trauma,shaken baby 37 A esophageal varices liver cirrhosis -->portal hypertension -->Ascites, splenomegaly, esophageal varices, caput medusae, haemarrhoids 38 B Zona glomerulosa -->Aldosterone other options C -zona fasciculata, D -zona reticularis, E -adrenal medulla 39.BB Diabetic retinopathy is retinopathy (damage to the retina) caused by complications of diabetes mellitus, which can eventually lead to blindness. It is an ocular manifestation of systemic disease which affects up to 80% of all patients who have had diabetes for 10 years or more. Diabetic retinopathy is the result of microvascular retinal changes. Hyperglycemia-induced intramural pericyte death and thickening of the basement membrane lead to incompetence of the vascular walls. These damages change the formati |
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