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  #101  
Old 11-16-2014
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Post Hi

Found many quick quiz aswer on : http://quizlet.com/44294470/nbme-16-flash-cards/

Intoxication with opiods: sxs pupillary constriction, euphoria, CNS depression
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Intoxication with amphetamines: sxs pupillary dilation, euphoria, anorexia, fever, HTN
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Lateral corticospinal tract decussates where? pyramids
damage BELOW ie in the spinal cord will result in ipsilateral sxs
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Bacterial transformation Ability for bacteria to take up naked DNA from environment
who can do it? S. pneumo, Hib, Neisseria
if you add DNAse, will degrade naked DNA and no transformation occurs
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pyruvate kinase: substrate and product substrate: PEP
product: pyruvate
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PFK-1: substrate and product substrate: Fructose-6-P
product: Fructose-1,6-BP
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Glyceraldehyde-3-phosphate dehydrogenase: substrate and product Substrate: glyceraldehyde 3 P
Product: 1,3 -bisphosphoglycerate
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Prader Willi- genetics most common is maternal imprining (paternal deletion)
OR less commonly materal origin of both chromosomes (maternal uniparental disomy)
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Roundworms Enterbius vermicularis
Ascaris lumbricoides
Strongyloides
Necantor
Ancylostoma
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First order kinetics same fraction is lost per unit time
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Zero order kinetics same amount is lost per unit time
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indomethacin MOA inhibit COX. dddduuuuuhhh
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Most frequent site of cardiac involvement in rheumatoid arthritis pericardium
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shunt vs dead space SHUNT= airway obstruction (V/Q=0)
DEAD SPACE= blood flow obstruction (V/Q=infinity)
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Horseshoe kidney- associated anomalies? D/t halted ascent, the renal vascular anomalies are common, and renal arteries do not arise from their normal level. Other complications include
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Fanconi syndrome Resorptive defect in the renal PCT. A/w overexcretion of AA, glucose, HCO3-, and Phos
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Bartter syndrome Resorptive defect in thick ascending limb of kidney. A/w hypokalemia, metabolic alkalosis, hypercalcuria
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Gitelman syndrome Resorptive defect in the DCT of the kidney. Hypokalemia and metabolic alkalosis (no hypercalcuria)
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Liddle syndrome Increased resorption of Na+ in the distal and collecting tubules (increased ENac activity). A/w hypernatremia, hypokalemia, metabolic alkalosis, HTN.

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Pulmonary surfactant is assembled/packaged for secretion in what part of type II pneumocytes? Lamellar bodies (indicated by arrows in pic)

Anti-proteinase 3 c=ANCA in Wegners is directly specifically against proteinase 3, found in cytoplasm of neutrophils
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microglia vs astrocytes microglia= macrophages of the CNS astrocytes= repair, physical support, reactive gliosis
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Mesna Reverse cyclophosphamide toxicity. Coadminister to prevent hemorrhagic cystitis
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Amifostine free radial scavenger. use for prevention of nephrotoxicty in pt taking cisplatin

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Kallkrein -requires Hagemen factor (XIIa) to be activated -activates conversion of HMWK to bradykinin and also plasminogen to plasmin

Nevirapine NNRTI (non nucleoside reverse transcriptase inhibitor).

Atrophy Occurs via ATP-dependent ubiquitin-proteasome pathway. Degrades damaged/unneeded proteins.
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  #102  
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Save It! Hi

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Originally Posted by sashabeliimd View Post
A 5 year old boy with mental retardation is grossly obese and has features of prader willi syndrome. Karyotipind and fluorescent in situ hybridization studies do not show deletion in the usual site on chromosome 15. Which of the following findings is most likely to confirm PWS in this child?

DEletion in the short arm of chromosome 15
Duplication within chromosome 15
Large trinucleotide repeat expansion in the PWS area of chromosome 15
Maternal origin of both chromosome 15
Translocation in the short arm of chromosome 15
In about 25 percent of cases, people with Prader-Willi syndrome inherit two copies of chromosome 15 from their mother instead of one copy from each parent. This phenomenon is called maternal uniparental disomy
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  #103  
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Originally Posted by sashabeliimd View Post
Potential fo a false positive result???????

Because test may be positive also for another diseases

Causes of Blood in Stool
Blood in the stool means there is bleeding somewhere in your digestive tract. Sometimes the amount of blood is so small that it can only be detected by a fecal occult test (which checks for hidden blood in the stool). At other times it may visible on toilet tissue or in the toilet after a bowel movement as bright red blood. Bleeding that happens higher up in the digestive tract may make stool appear black and tarry.

Possible causes of blood in stool include:

Diverticular disease. Diverticula are small pouches that project from the colon wall. Usually diverticula don't cause problems, but sometimes they can bleed or become infected.


Anal fissure . A small cut or tear in the tissue lining the anus similar to the cracks that occur in chapped lips or a paper cut. Fissures are often caused by passing a large, hard stool and can be painful.

Colitis . Inflammation of the colon. Among the more common causes are infections or inflammatory bowel disease.

Angiodysplasia. A condition in which fragile, abnormal blood vessels lead to bleeding.

Peptic ulcers . An open sore in the lining of the stomach or duodenum, the upper end of the small intestine. Many peptic ulcers are caused by infection with a bacterium called Helicobacter pylori (H. pylori). Long-term use or high doses of anti-inflammatory drugs such as aspirin, ibuprofen, and naproxen can also cause ulcers.

Polyps or cancer . Polyps are benign growths that can grow, bleed, and become cancerous. Colorectal cancer is the third most common cancer in the U.S. It often causes bleeding that is not noticeable with the naked eye.

Esophageal problems. Varicose veins of the esophagus or tears in the esophagus can lead to severe blood loss.
You consider specificity and specificity in choosing a diagnostic order. So probably the correct answer here is low sensitivity. That is what you want anyway in any screening exam...
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  #104  
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Originally Posted by sashabeliimd View Post
Prader-Willi syndrome
Prader-Willi syndrome is caused by a loss of active genes in a region of chromosome 15. This region is located on the long (q) arm of the chromosome and is designated 15q11-q13. It is the same part of chromosome 15 that is usually affected in people with Angelman syndrome, although different genes are associated with the two disorders. People can have either Prader-Willi syndrome or Angelman syndrome, but they typically cannot have both.
People normally inherit one copy of chromosome 15 from each parent. Some genes on this chromosome are turned on (active) only on the copy inherited from a person's father (the paternal copy). This parent-specific gene activation results from a phenomenon called genomic imprinting.
In about 70 percent of cases, Prader-Willi syndrome occurs when the 15q11-q13 region of the paternal chromosome 15 is deleted in each cell. A person with this chromosomal change will be missing certain critical genes in this region because the genes on the paternal copy have been deleted, and the genes on the maternal copy are turned off (inactive). Researchers are working to identify which missing genes are associated with the characteristic features of Prader-Willi syndrome.
In about 25 percent of cases, people with Prader-Willi syndrome inherit two copies of chromosome 15 from their mother instead of one copy from each parent. This phenomenon is called maternal uniparental disomy. A person with two maternal copies of chromosome 15 will have no active copies of certain genes in the 15q11-q13 region.
In a small percentage of cases, Prader-Willi syndrome is caused by a chromosomal rearrangement called a translocation. Rarely, the condition results from a mutation or other defect that abnormally inactivates genes on the paternal copy of chromosome 15.



People normally inherit one copy of chromosome 15 from each parent How can child have both copies if receive one copy from mother and another from father, and if one will be inactivated like paternal chromosome 15, he will remain just with one maternal 15 not, both ?????
Please dont write more some of this sh.............ty posts without comments to them... thanks


sorry...instead of mentioning just, imprinting.....i should have said more about it.
Prader Willi syndrome : gene from mom is normally silent and paternal gene is deleted.
25% of cases are due to maternal uniparental disomy (2 maternally imprinted genes are received; no paternal gene is received)
given in FA, page 85

hey Shashabeliimd, though not completely.....but to some extent, this thread helped me....thanks...all the best
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  #105  
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Info Hi

A 64 year old man is evaluated for cough, dyspnea and chest pain. He is afebrile . An x ray fo the chest shows an abnormal density in the hilar region. Lung tissue biopsy shows round cells with a little cytoplasm that are about twice the size of lymphocytes. These cells are arranged in infiltrating sheets that have neither glandular nor squamous organization. Which of the following abnormalities in serum is most likely in this patient?

Hyperkalemia

Hyperlipidemia

Hypermagnesemia wrongggggggggg

Hypoalbuminemia

Hypoglycemia

Hyponatremia
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  #106  
Old 11-17-2014
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Quote:
Originally Posted by sashabeliimd View Post
A 64 year old man is evaluated for cough, dyspnea and chest pain. He is afebrile . An x ray fo the chest shows an abnormal density in the hilar region. Lung tissue biopsy shows round cells with a little cytoplasm that are about twice the size of lymphocytes. These cells are arranged in infiltrating sheets that have neither glandular nor squamous organization. Which of the following abnormalities in serum is most likely in this patient?

Hyperkalemia

Hyperlipidemia

Hypermagnesemia wrongggggggggg

Hypoalbuminemia

Hypoglycemia

Hyponatremia

Its not Squamous nor glandular (so its not adeno), what else do we have? well, small cell ca, that can produce ADH, and we will have hyponatremia.
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  #107  
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Originally Posted by sashabeliimd View Post
A 19 year old woman is brought to the physician be her mother because she has been increasingly withdrawn and isolated since graduating from high school 1 year ago. The mother reports that the patien stays in her bedroom much of the time and rarely sees friends. The patient says that she is not interested in her old friends or activities.
She has been anxious and depressed about what she has learned by listening to radio broadcasts that only she can hear. She has been spending most of her time thinking about a government scheme to control th physic pain feel. She does not dring alcohol or use ilicit drugs. She appears disheveld and is malodorous. Vital signs are within normal limits. Physical examinatino shows no abnormalities. On mental status examination, she is distracted. She has a sad mood and an anxious , sad, and blunted affect. She is oriented to person place and time. Which of the following is the most appropiate pharmacotherapy?


Buspirone wrong
Donepezil
LIthium carbonate
Risperidone
Trazodone


Please hepl to establish diagnosis for first, and wich drug can be use for this state treatment???
Patient has Schizophrenia, disorganized type.

Buspirone is anxiolytic, Lithium is for mania of bipolar, Donepezil is anticholinergic for Alzheimer, Trazodone is atypical antidepressant

Thus Risperidone is the only drug left... and its an atypical antidepressant
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  #108  
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Correct Answer Hi

Quote:
Originally Posted by Coccidioda View Post
Its not Squamous nor glandular (so its not adeno), what else do we have? well, small cell ca, that can produce ADH, and we will have hyponatremia.


Syndrome of inappropriate antidiuretic hormone production (SIADH)
See Hyponatremia in Nephrology for details
Ectopic secretion of ADH → retain free water in collecting ducts
Euvolemic hyponatremia and concentrated urine
Mild symptoms include headache and weakness, severe symptoms include altered mental status, seizures, respiratory depression, and death
Common in SCLC
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  #109  
Old 11-17-2014
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Drug NBME

Hantavirus strain A grows poorly at a temperature of 39 C. Whereas hantavirus strain B displays normal growth at that temperature. Hantaviruses contain a genome consisting of three RNA segments termed large L, medium M, small S. To identify viral genes that segregate with the growth differences of hantavirus A and hantavirus B at 39 C , hantavirus A x hantavirus B reassortant viruses are isolated by coinfecting cells with both virus strains. Growth of each of the reassortant viruses at 39 C is shown in the table...

Look table below...

Which of the following viral gene segments is associated with the temperature sensitive phenotype of hantavirus strain A?

L
M
S
All three gene segments contribute to temperature sensitivity wrrrrrrrrrrrong
None of the gene segments contributes to temperature sensitivity

please help, i don't understand this quetions, somebody explane in simple language...
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  #110  
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Post nbme

A 23 year old man comes to the emergency department because of a 2 week history of back pain refractory to treatment with over-the-counter medications. He demands a prescription for an opioid drug because they're only medication that decrease my pain. He becomes upset when he is told that over the counter medications should relieve his symptoms. His temperature is 37 pulse is 70, and respirations are 18, and BP is 120/70. Physical examination shows no abnormalities , Which of the following is the most appropiate action by the physician.?

Determine which drugs have been prescribed for the patient in the past

OBtain serum toxicology screening on the patient

Order an MRI of the spine wrrrrrrrrong

Prescribe only a 2 week course of a narcotic medication for the patient

Refer the patient to a drug addiction program
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  #111  
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Quote:
Originally Posted by sashabeliimd View Post
Hantavirus strain A grows poorly at a temperature of 39 C. Whereas hantavirus strain B displays normal growth at that temperature. Hantaviruses contain a genome consisting of three RNA segments termed large L, medium M, small S. To identify viral genes that segregate with the growth differences of hantavirus A and hantavirus B at 39 C , hantavirus A x hantavirus B reassortant viruses are isolated by coinfecting cells with both virus strains. Growth of each of the reassortant viruses at 39 C is shown in the table...

Look table below...

Which of the following viral gene segments is associated with the temperature sensitive phenotype of hantavirus strain A?

L
M
S
All three gene segments contribute to temperature sensitivity wrrrrrrrrrrrong
None of the gene segments contributes to temperature sensitivity

please help, i don't understand this quetions, somebody explane in simple language...

the question is simple if you read carefully, it says that at 39 A is sensitive, so first of all you are going to check which ones didn't grow (which are sensitive), the negative at the end, those would be row 1, 4 and 6. Then you check where hantavirus A appears ALWAYS, that would be in the LARGE strain. So the answer here would be L.
Hope this helps
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  #112  
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Quote:
Originally Posted by sashabeliimd View Post
A 23 year old man comes to the emergency department because of a 2 week history of back pain refractory to treatment with over-the-counter medications. He demands a prescription for an opioid drug because they're only medication that decrease my pain. He becomes upset when he is told that over the counter medications should relieve his symptoms. His temperature is 37 pulse is 70, and respirations are 18, and BP is 120/70. Physical examination shows no abnormalities , Which of the following is the most appropiate action by the physician.?

Determine which drugs have been prescribed for the patient in the past

OBtain serum toxicology screening on the patient

Order an MRI of the spine wrrrrrrrrong

Prescribe only a 2 week course of a narcotic medication for the patient

Refer the patient to a drug addiction program
MRI is too expensive to be the first thing to do, you cant asume he is a junkie by obtaining his toxicology, of course you are not going to give him narcotics right away, and you NEVER refer a patient (at least not on step1 questions ) So the only one left would be our right answer, to determine which drugs he was given in the past. I did this one by ruling out the other ones, not that it made a lot of sense to me.
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  #113  
Old 11-17-2014
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Correct Answer Hi

Quote:
Originally Posted by Coccidioda View Post
MRI is too expensive to be the first thing to do, you cant asume he is a junkie by obtaining his toxicology, of course you are not going to give him narcotics right away, and you NEVER refer a patient (at least not on step1 questions ) So the only one left would be our right answer, to determine which drugs he was given in the past. I did this one by ruling out the other ones, not that it made a lot of sense to me.
Thanks for reply, I know that rule out another variant often may help us to answer, some rules right here like, do not redirect patient to another physician,
or do not give morphine, opioids for every patient who want to take them, because it's a group of special drugs, and may lead to narcomania,


Thanks again for a quick reply..........
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  #114  
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Correct Answer nbme

A couple seeks genetic counseling because of a family history of fragile X syndrome as shown in the pedigree. Affected individuals are indicated by shading . Individuals I-1 and I-2 undergo DNA based testing for the FMR1 gene. if individual I-2 is found to have an expansion of FMR-1 gene, which of the following is the approximate likelihood that individual III-5 has similar exapansion of the gene?


O %%%
25%%%%
50 %%% wronggggggggg
75%%%%
100%%%%
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  #115  
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Post NBME

A 19 year old wommmmmmmmman is brougth to the physician by her mother because she has been increasingly withdrawan and isolated since graduating from high school 1 year ago. The mother reports that the patient stays in her bedroom much of the time and rarely sees friends. The patient says that she is not interested in her old friends or activities . She has been anxious and depressed about what she has learned by listening to radio broadcasts that only she can hear. She has been spending most of her time thinking about a government scheme to control the psychic pain people feel. She does not drink alcohol or use illicit drugs. She appears disheveled and is malodorous . Vital signs are within normal limits. Physical examination shows no abnormalities. On mental status examination, she is distracted .She has a sad mood and an anxious , sad, adn blunted affect. She is oriented to person place, and time,
Which of the following is the most appropiate pharmacotherapy?

Diagnosis i think is schyzophrenia, simple type or ( where persons do not care about their healthy, hygiene, and wearing....

Buspirone wrrrrrrrrrrrrrrrrrong

Donepezil noooooo

LIthium carbonate

Risperidone

Trazodone

Tx will be with atypical antipsychotics? like risperidone? please explane someone right way....

Last edited by ginseng plus; 11-18-2014 at 01:21 AM.
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  #116  
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Default HEY

Quote:
Originally Posted by sashabeliimd View Post
A 19 year old wommmmmmmmman is brougth to the physician by her mother because she has been increasingly withdrawan and isolated since graduating from high school 1 year ago. The mother reports that the patient stays in her bedroom much of the time and rarely sees friends. The patient says that she is not interested in her old friends or activities . She has been anxious and depressed about what she has learned by listening to radio broadcasts that only she can hear. She has been spending most of her time thinking about a government scheme to control the psychic pain people feel. She does not drink alcohol or use illicit drugs. She appears disheveled and is malodorous . Vital signs are within normal limits. Physical examination shows no abnormalities. On mental status examination, she is distracted .She has a sad mood and an anxious , sad, adn blunted affect. She is oriented to person place, and time,
Which of the following is the most appropiate pharmacotherapy?

Diagnosis i think is schyzophrenia, simple type or ( where persons do not care about their healthy, hygiene, and wearing....

Buspirone wrrrrrrrrrrrrrrrrrong

Donepezil noooooo

LIthium carbonate

Risperidone

Trazodone

Tx will be with atypical antidepressants? like risperidone? please explane someone right way....
She has all the symptoms of a schizophrenic thats why.. >1 year, listening to voices, etc,
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  #117  
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Quote:
Originally Posted by sashabeliimd View Post
A 19 year old wommmmmmmmman is brougth to the physician by her mother because she has been increasingly withdrawan and isolated since graduating from high school 1 year ago. The mother reports that the patient stays in her bedroom much of the time and rarely sees friends. The patient says that she is not interested in her old friends or activities . She has been anxious and depressed about what she has learned by listening to radio broadcasts that only she can hear. She has been spending most of her time thinking about a government scheme to control the psychic pain people feel. She does not drink alcohol or use illicit drugs. She appears disheveled and is malodorous . Vital signs are within normal limits. Physical examination shows no abnormalities. On mental status examination, she is distracted .She has a sad mood and an anxious , sad, adn blunted affect. She is oriented to person place, and time,
Which of the following is the most appropiate pharmacotherapy?

Diagnosis i think is schyzophrenia, simple type or ( where persons do not care about their healthy, hygiene, and wearing....

Buspirone wrrrrrrrrrrrrrrrrrong

Donepezil noooooo

LIthium carbonate

Risperidone

Trazodone

Tx will be with atypical antidepressants? like risperidone? please explane someone right way....
I'm am sorry... But Risperidone is an atypical antipsychotic. I previously said it's an antidepressant
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  #118  
Old 11-18-2014
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Post Hi

Quote:
Originally Posted by coelom View Post
I'm am sorry... But Risperidone is an atypical antipsychotic. I previously said it's an antidepressant
it's ok, atypical antipsychotic of course important is that you give a corect idea...
What about quetion with x linked syndrome (X fragile ),
50% will receive disease, and if yet 50% of children have disease, then chance to another half will be 0%?????
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  #119  
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I don't quite understand the question either. Besides, if you look at II-2, II-3, and II-6, how can they spawn offsprings on their own? What is the genotype of their husbands?

Anyway, since it's an X-linked disease, and the index patient is female, One X should come from the father, and another from the mother. In short, She should have 50% chance of carrying the mutation...
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  #120  
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I disagree Hi

Quote:
Originally Posted by coelom View Post
I don't quite understand the question either. Besides, if you look at II-2, II-3, and II-6, how can they spawn offsprings on their own? What is the genotype of their husbands?

Anyway, since it's an X-linked disease, and the index patient is female, One X should come from the father, and another from the mother. In short, She should have 50% chance of carrying the mutation...
Recurrence risks for X linked recessive diseases will be:
50% transmision for sons of disease, and half of sons will have disease, half of the doughters will be carriers...

50% is incorect here
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  #121  
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Originally Posted by sashabeliimd View Post
Recurrence risks for X linked recessive diseases will be:
50% transmision for sons of disease, and half of sons will have disease, half of the doughters will be carriers...

50% is incorect here

Okay. I got it. There should be no Male-to-Male transfer in an X-linked trait. So there is no way III-5 will have the mutation.

The answer should be 0%
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  #122  
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Correct Answer Hi

Quote:
Originally Posted by coelom View Post
Okay. I got it. There should be no Male-to-Male transfer in an X-linked trait. So there is no way III-5 will have the mutation.

The answer should be 0%
Because sons will receive X chromosome from mother, and if father is affected, transmition to him son will be near or right 0.
Thanks for deducing right one...
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  #123  
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Correct Answer Behavioral

A 60 year old woman with a 2 year history of hypertension comes to the physician for a follow up examination. Her hypertension has been poorly controlled during the past 6 months despite availability of appropiate pharmacotherapy. Which of the following statements by the physician is most appropiate to begin a discussion about this patient's possible noncompliance with her medication regimen?

I will arrange for a nurse to visit you every day to make sure that you are taking your medication properly

I'm sorry, but i must tell you that missing your medication could kill you ????

It is hard to take a pills every day for a condition that has no symptoms

YOu clearly have not been taking your medication, You must be more responsible Wrrrrrrrrrrrrrrroooooooooooooooongggggggggggg

You realize that you high blood pressure could have been avoided


I think aswer is to tell to patient reality, about medication, effect, and no taking medication that may result in death.
Wait your explanation guys.. thanks
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Quote:
Originally Posted by sashabeliimd View Post
A 60 year old woman with a 2 year history of hypertension comes to the physician for a follow up examination. Her hypertension has been poorly controlled during the past 6 months despite availability of appropiate pharmacotherapy. Which of the following statements by the physician is most appropiate to begin a discussion about this patient's possible noncompliance with her medication regimen?

I will arrange for a nurse to visit you every day to make sure that you are taking your medication properly

I'm sorry, but i must tell you that missing your medication could kill you ????

It is hard to take a pills every day for a condition that has no symptoms

YOu clearly have not been taking your medication, You must be more responsible Wrrrrrrrrrrrrrrroooooooooooooooongggggggggggg

You realize that you high blood pressure could have been avoided


I think aswer is to tell to patient reality, about medication, effect, and no taking medication that may result in death.
Wait your explanation guys.. thanks

You Never scare a patient! and you never tell him/her that he is not taking his pills because you actually dont know if she is or not, there could be a million reasons why the med is not working or if shes not taking them you just let her tell you.
You just have to show empathy and let her tell you if she is taking them or not.. (It is hard to take a pills every day for a condition that has no symptoms)
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  #125  
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Originally Posted by Coccidioda View Post
You Never scare a patient! and you never tell him/her that he is not taking his pills because you actually dont know if she is or not, there could be a million reasons why the med is not working or if shes not taking them you just let her tell you.
You just have to show empathy and let her tell you if she is taking them or not.. (It is hard to take a pills every day for a condition that has no symptoms)
Thank you very much for this great explanation...

Principal idea to memorise here is patient is all, and you must ask him, porpose but do not harm, ingore, ordone, and other tasks,,,

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  #126  
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Correct Answer

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Originally Posted by coelom View Post
Patient has Schizophrenia, disorganized type.

Buspirone is anxiolytic, Lithium is for mania of bipolar, Donepezil is anticholinergic for Alzheimer, Trazodone is atypical antidepressant

Thus Risperidone is the only drug left... and its an atypical antipsychotic


Just want to mention some of the important diagnosis related to psychiatry

Schizotypal
Personality disorder with interpersonal awkwardness, odd thoughts, odd apearance, strange behavior

Schizophrenia
Delusions or hallucinations
+/- negative symptoms
more than 6 months

Schizoaffective
Schizophrenia symptoms plus mood disorder

Schizoid
Personality disorder with voluntary social withdrawal

Schizophreniform
Schizophrenia symptoms that last more than 1 month but fewer than 6 months
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  #127  
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Emergency Neurology

A 16 year old boy is brought to the emergency department 30 minutes after he dove into a 3 food deep swimming pool at night. On examination, he is unable to move the right and lower extremities. The most likely cause of the movement deficits in this patient is damage to which of the following labeled regions in the photograph of a cross section of the spinal cord shown?

This must be attached to corticospinal tract, but still dont catch right answer....
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  #128  
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Default hey

Quote:
Originally Posted by sashabeliimd View Post
A 16 year old boy is brought to the emergency department 30 minutes after he dove into a 3 food deep swimming pool at night. On examination, he is unable to move the right and lower extremities. The most likely cause of the movement deficits in this patient is damage to which of the following labeled regions in the photograph of a cross section of the spinal cord shown?

This must be attached to corticospinal tract, but still dont catch right answer....
RIGHT CORTICOSPINAL E

A, B, C, D is Dorsal column, ipsilateral propioception, vibration etc..
E, F, corticospinal, ipsilateral motor
G, H, Spinothalamic CONTRAlateral pain/temp

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  #129  
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Quote:
Originally Posted by Coccidioda View Post
RIGHT CORTICOSPINAL E

A, B, C, D is Dorsal column, ipsilateral propioception, vibration etc..
E, F, corticospinal, ipsilateral motor
G, H, Spinothalamic CONTRAlateral pain/temp

This secion of spinal cort looks like a cervical portion...

Realy thanks for all your last replies, help in what i had doubts about quetions, just 3 more quetions to finish detailed review of my form nbme 16,,,
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  #130  
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Correct Answer Nbme 16

A 12 year old girl who recently immigrated to the USA from central africa is brought to the physician because of a 5 week history of increasingly severe abdominal pain and vomiting blood. Her temperature is 37.8, pulse is 110 and respirations 27 per minut. and blood pressure is 112/65 mm Hg. Physical examination shows hepatosplenomegaly and abdominal ascites. Laboratory studies shos:

Leukocyte count 13.4
Segmented 43%
Eosinophils 15%
LYMPHOCYTES 37%
Monocytes 6%

a PHOTOMICROGRAPH of a stool specimen is shown. Which of the following is the most appropiate pharmacotherapy for this patient?

Fluconazole noooo, it;s not a fungal infection

Levofloxacin noooo

Metronidazole wrrrrrrrrrrrrrrrroooooooooooong

Praziquantel may be

Trimethoprim- sulphamethoxazole

What for first is this detected infection?
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  #131  
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Quote:
Originally Posted by sashabeliimd View Post
A 12 year old girl who recently immigrated to the USA from central africa is brought to the physician because of a 5 week history of increasingly severe abdominal pain and vomiting blood. Her temperature is 37.8, pulse is 110 and respirations 27 per minut. and blood pressure is 112/65 mm Hg. Physical examination shows hepatosplenomegaly and abdominal ascites. Laboratory studies shos:

Leukocyte count 13.4
Segmented 43%
Eosinophils 15%
LYMPHOCYTES 37%
Monocytes 6%

a PHOTOMICROGRAPH of a stool specimen is shown. Which of the following is the most appropiate pharmacotherapy for this patient?

Fluconazole noooo, it;s not a fungal infection

Levofloxacin noooo

Metronidazole wrrrrrrrrrrrrrrrroooooooooooong

Praziquantel may be

Trimethoprim- sulphamethoxazole

What for first is this detected infection?
the picture is of a schistosoma, note the spike.. tx is praziquantel
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  #132  
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Romania Hi

Quote:
Originally Posted by sashabeliimd View Post
A 12 year old girl who recently immigrated to the USA from central africa is brought to the physician because of a 5 week history of increasingly severe abdominal pain and vomiting blood. Her temperature is 37.8, pulse is 110 and respirations 27 per minut. and blood pressure is 112/65 mm Hg. Physical examination shows hepatosplenomegaly and abdominal ascites. Laboratory studies shos:

Leukocyte count 13.4
Segmented 43%
Eosinophils 15%
LYMPHOCYTES 37%
Monocytes 6%

a PHOTOMICROGRAPH of a stool specimen is shown. Which of the following is the most appropiate pharmacotherapy for this patient?

Fluconazole noooo, it;s not a fungal infection

Levofloxacin noooo

Metronidazole wrrrrrrrrrrrrrrrroooooooooooong

Praziquantel may be

Trimethoprim- sulphamethoxazole

What for first is this detected infection?

Clonorchis sinensis, the Chinese liver fluke, is a human liver fluke in the class Trematoda, phylum Platyhelminthes. This parasite lives in the liver of humans, and is found mainly in the common bile duct and gall bladder, feeding on bile. These animals, which are believed to be the third most prevalent worm parasite in the world, are endemic to Japan, China, Taiwan, and Southeast Asia, currently infecting an estimated 30,000,000 humans.[1] 85% of cases are found in China.

It is the most prevalent human trematode in Asia, and still actively transmitted in Korea, China, Vietnam and also Russia, with 200 million people at constant risk. Recent studies have proved that it is capable of causing cancer of liver and bile duct, and in fact the International Agency for Research on Cancer has classed it as a group 1 biological carcinogen in 2009


If this is clonorchis sinensis how i think , about symptoms like affecting biliary tract, and cirrhosis wiil occur, then

Diagnosis and treatment[edit]
Infection is detected mainly on identification of eggs by microscopic demonstration in faeces or in duodenal aspirate. But other sophisticated methods have been developed such as ELISA which has become the most important clinical technique. Diagnosis by detecting DNAs from eggs in faeces are also developed using PCR, real-time PCR, and LAMP, which are highly sensitive and specific. Imaging diagnosis has been studied in depth and is now widely used.[2][10] Drugs used to treat infestation include triclabendazole, praziquantel, bithionol, albendazole, levamisole and mebendazole.However, benzimidazoles are very weak as vermicide. As with other trematodes, praziquantel is the drug of choice. Lately, tribendimidine has been acknowledged as an effective and safe drug


Mebendazole is a good option, but because is absent as option on quetion, second most useful ithink will be praziquantel
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  #133  
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Correct Answer Hi

Quote:
Originally Posted by Coccidioda View Post
the picture is of a schistosoma, note the spike.. tx is praziquantel
What do you mean with SPIKE? about increased Eosinophils???
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  #134  
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Default Hi

Quote:
Originally Posted by Coccidioda View Post
the picture is of a schistosoma, note the spike.. tx is praziquantel
You are about this spike?
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Default yes

Quote:
Originally Posted by sashabeliimd View Post
You are about this spike?
yes, search for pictures of schistosoma, youll see it..
could be schistosoma mansoni

The clinical presentation can be a lot of things, but the picture is what is what gives it away
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Default FA

Quote:
Originally Posted by Coccidioda View Post
yes, search for pictures of schistosoma, youll see it..
could be schistosoma mansoni
go to page 152, FA 2013.. parasite hints.. schistosoma mansoni = portal hypertension, google it for pics
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  #137  
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Post Hi

ok i got it thanks

https://www.google.md/search?q=schis...w=1366&bih=600
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Post Hi

AN 18 month old boy is brought to the emergency department because of lethargy for 3 hours. He has not eaten well for the past 24 hours. He had cardiorespiratory arrest associated with hypoglycemia after an episode of diarrhea 10 months ago. On arrival he is unresponsive. His temperature is 37, pulse is 140, and respiratory rate is 25, BP 100/60 mm Hg. Physical examination shows hepatomegaly. Laboratory studies show.


Following intravenous administration of glucose he becomes responsive. Medium chain triglycerides are administered daily for 6 months. At a follow up examination his serum glucose concentration is within the reference range. A deficiency of which of the following enzymes is the most likely cause of these findings?


Glucose 6 phosphatase

HMG coA lyase

Hormone sensitive lipase

Lipoprotein lipase wrrrrrrrrrrrrrrrrrrrroooooooooooong

Long chain acyl CoA dehydrogenase

Phosphoenolpyruvate carboxykinase

I know one thing , than gluconeogenesis here is impared, if administration of glucose improve patient responsivness.
Which enzyme and pathway please explane. thanks
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Quote:
Originally Posted by sashabeliimd View Post
AN 18 month old boy is brought to the emergency department because of lethargy for 3 hours. He has not eaten well for the past 24 hours. He had cardiorespiratory arrest associated with hypoglycemia after an episode of diarrhea 10 months ago. On arrival he is unresponsive. His temperature is 37, pulse is 140, and respiratory rate is 25, BP 100/60 mm Hg. Physical examination shows hepatomegaly. Laboratory studies show.


Following intravenous administration of glucose he becomes responsive. Medium chain triglycerides are administered daily for 6 months. At a follow up examination his serum glucose concentration is within the reference range. A deficiency of which of the following enzymes is the most likely cause of these findings?


Glucose 6 phosphatase

HMG coA lyase

Hormone sensitive lipase

Lipoprotein lipase wrrrrrrrrrrrrrrrrrrrroooooooooooong

Long chain acyl CoA dehydrogenase

Phosphoenolpyruvate carboxykinase

I know one thing , than gluconeogenesis here is impared, if administration of glucose improve patient responsivness.
Which enzyme and pathway please explane. thanks
I think the absence of ketosis at time of hypoglycemia points to a fatty acid metabolism problem. So if I would have to choose, then its long chain acyl coA dehydrogenase.

Additional clue would be a good clinical response to Medium chain triglycerides
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I think the absence of ketosis at time of hypoglycemia points to a fatty acid metabolism problem. So if I would have to choose, then its long chain acyl coA dehydrogenase.

Additional clue would be a good clinical response to Medium chain triglycerides

totally agree, hypoglycemia with hypoketosis, classic presentation for medium chain acyl coa dh def, since medium is not there, i will go with long chain
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Correct Answer

Quote:
Originally Posted by Coccidioda View Post
totally agree, hypoglycemia with hypoketosis, classic presentation for medium chain acyl coa dh def, since medium is not there, i will go with long chain
Thus, the two substrates of this enzyme are acyl-CoA and acceptor, whereas its two products are 2,3-dehydroacyl-CoA and reduced acceptor.

This enzyme belongs to the family of oxidoreductases, specifically those acting on the CH-CH group of donor with other acceptors. The systematic name of this enzyme class is long-chain-acyl-CoA:acceptor 2,3-oxidoreductase. Other names in common use include palmitoyl-CoA dehydrogenase, palmitoyl-coenzyme A dehydrogenase, long-chain acyl-coenzyme A dehydrogenase, and long-chain-acyl-CoAacceptor) 2,3-oxidoreductase. This enzyme participates in fatty acid metabolism and ppar signaling pathway. It employs one cofactor, FAD.

Mitochondrial mutations in this enzyme may be associated with some forms of dilated cardiomyopathy.



What is VLCAD deficiency?
Very long-chain acyl-CoA dehydrogenase (VLCAD) deficiency is a condition that prevents the body from converting certain fats to energy, particularly during periods without food (fasting).

Signs and symptoms of VLCAD deficiency typically appear during infancy or early childhood and can include low blood sugar (hypoglycemia), lack of energy (lethargy), and muscle weakness. Affected individuals are also at risk for serious complications such as liver abnormalities and life-threatening heart problems. When symptoms begin in adolescence or adulthood, they tend to be milder and usually do not involve the heart.
Problems related to VLCAD deficiency can be triggered by periods of fasting, illness, and exercise. This disorder is sometimes mistaken for Reye syndrome, a severe disorder that may develop in children while they appear to be recovering from viral infections such as chicken pox or flu. Most cases of Reye syndrome are associated with the use of aspirin during these viral infections.
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Default Last one

A new antiplatelet agent is developed for the prevention of recurrence of stronke. In a large randomized clinical trial with equal numbers of men and women, the rates of stroke are lower in patients receiving the new agent than in patients receiving the standard treatment.
Results are shown:

Based on the results, which of the following is the absolute risk reduction in women?

IN percents %

8
12
16
33
50
62
67 wrong
75
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  #143  
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Default ARR

Quote:
Originally Posted by sashabeliimd View Post
A new antiplatelet agent is developed for the prevention of recurrence of stronke. In a large randomized clinical trial with equal numbers of men and women, the rates of stroke are lower in patients receiving the new agent than in patients receiving the standard treatment.
Results are shown:

Based on the results, which of the following is the absolute risk reduction in women?

IN percents %

8
12
16
33
50
62
67 wrong
75
ARR= event rate in Control - event rate in Treatment

ARR= 0.12 - 0.04 = 0.08 since is in % multiply by 100 = 8%
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  #144  
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Thumbs Up Finish

Finaly , was creaated a nice thread, where anyone can find exact what are looking for, i want to say thanks for all who participate in discussion here, and add some precious info....
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  #145  
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Romania Hi

Quote:
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A male newborn delivered at 28 weeks gestation is tachypneic and hypoxemic. Which of the following altered structure changes in the type 2 pneumocytes is the most likely cause of this patient's condition?

Abundant rought endoplasmic reticulum wrong
Decreased numbers of lamellar bodies
Distinct junctional complexes with adjacent type 1 pneumocytes
NUmerous microvilli
Reticular fibers


I would like to say that , all this i do for myself primarily, but if someone find interesting , you are welcome...

Prior 35 weeks of gestaion, newborn have deficient surfactant secretion...
Acute respiratory distress syndrome

May be caused by trauma , sepsis , shock, gastric aspiration, uremia ,a acute pancreatitis, or amniotic fluid embolism. Diffuse alveolar damage, INcrease alveolar permeability capilary, protein rich leakage into alveoli. Resaults in formation of intra-alveolar hyaline menmbrane.
Initial damage due to release of neutrophilic substances toxic to alveolar wall, activation of coagulation cascade, and oxygen derived free radicals,...


Microvilli aren't present on terminal alveoli

I think it is Distinct junctional complexes with adjacent type 1 pneumocytes

If someone have corect answer post please....
I found that pneumocytes of type 2 is deposited in the lamellar bodies


Lamellar granules (otherwise known as membrane-coating granules (MCGs), lamellar bodies, keratinosomes or Odland bodies) are secretory organelles found in type II pneumocytes and keratinocytes. They are oblong structures, appearing about 300-400 nm in width and 100-150 nm in length in transmission electron microscopy images. Lamellar granules fuse with the cell membrane and release their contents into the extracellular space.[1]
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It's clear that diagnosis is a cystic fibrosis
BUt a pathogenesis of CF consist by an abnormal traficking of a transmembrane protein.
Mutation causes abnormal protein folding, resulting in degradation of channel before reaching cell surface.
Protein stucture May somebody verify if i deduce a corect answer???
Yes protein structure is correct. I marked it and did not see it in the expanded feedback.
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Quote:
Originally Posted by coelom View Post
I think the absence of ketosis at time of hypoglycemia points to a fatty acid metabolism problem. So if I would have to choose, then its long chain acyl coA dehydrogenase.

Additional clue would be a good clinical response to Medium chain triglycerides
Yup. I got this one right.
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A male newborn delivered at 28 weeks gestation is tachypneic and hypoxemic. Which of the following altered structure changes in the type 2 pneumocytes is the most likely cause of this patient's condition?

Abundant rought endoplasmic reticulum wrong
Decreased numbers of lamellar bodies
Distinct junctional complexes with adjacent type 1 pneumocytes
NUmerous microvilli
Reticular fibers
..
The correct answer is Decreased no of lamellar bodies.
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Because all genes are synthesized in the nucleus ,fits last answer, with
transport of ferritin mRNA out of the nucleus

Please help someone to confirm this one....
Hey ! the answer was increase in translation i got it right.
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This boy have hepatitis after adminisration of ASPIRIN

Summary
Viral encephalitis is inflammation of the brain caused by a virus. The major risk from viral meningitis is permanent brain damage. Children aged one year or less and adults aged 55 years and over are more vulnerable to life threatening complications. Viruses that can cause encephalitis include enteroviruses such as poliovirus and echovirus, herpes simplex virus, varicella-zoster virus, Epstein-Barr virus, cytomegalovirus, adenovirus, rubella, measles, Murray Valley encephalitis (MVE) virus, Kunjin virus and Japanese encephalitis virus.

Symptoms

The symptoms of viral encephalitis include:
High temperature
Headache
Sensitivity to light (photophobia)
General malaise
Stiff neck
Stiff back
Vomiting
Changes to personality
Confusion
Memory loss (amnesia)
Seizures
Paralysis
Coma.
i choose e and its wrong ?
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Originally Posted by ginseng plus View Post
A 35 y o man comes to the physician because of a 3 year history of an enlarging nose, coarsening of his facial features, musle weakness, and increased hand and foot size. Physical examination shows a large fleshy nose and prognathism. Serum studies shows an increased insulin-like growth factor 1 concentration. An MRI of the brain shows a pituitary adenoma. Morphologic analysis of a biopsy specimen of the tumor shows a densely granulated somatotroph adenoma. Further studies show that the G alpha s, subunit of G proteins in the tumor lack GTPase activity. The tumor cells in this patient most likely have an increased activity of which of the following enzymes?

Adenylyl cyclase
Guanylyl cylcase
Janus kinase wrooooooooooong
Phospholipase C
Tyrosine kinase
GHRH works through Gs-cAMP pathway, if the patient is secreting excessive amounts of GH, it means that the pathway is working extra hours.

If you see the image of the pathway, the NEXT enzyme after the "G-protein complex" is adenylyl cyclase, so that should have an increased activity
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  #152  
Old 04-13-2016
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Check out testpirates for nbme 16 answers coming soon by the end of this week! as well as explanations Enjoy!
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  #153  
Old 05-29-2016
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Quote:
Originally Posted by ginseng plus View Post
It's very important tu understand in every NBME what they want from us to know

It's a classic features of gigantism, enlarged nose, hands, feet.
Occur in adult people, problem is with increased Growth hormone secretion,
I'am not discovering here nothing new, just try to analyze some quetions...

Insulin like peptide is increased, which work through tyrosine kinase receptor.
I marked tyrosine kinase and it's wrong ..
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  #154  
Old 06-03-2016
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Quote:
Originally Posted by ginseng plus View Post
A 5 year old boy is brought to the emergency department because of a 16 hour history of severe vomiting and increased sleepiness. His mother says that he had a flulike illness 5 days ago that she treated with aspirin. Shortly after admission, he becomes delirious and then comatose.... His prothrombin time is prolonged. Serum studies show increased ammonia and lactate concentration and increased transaminase activities. Which of the following is the most likely cause of this patients coma?

Cerebral edema
Metabolic alkalosis
Subarachnoid hemorrhage wronggggggggg
venous sinus thrombosis
viral encephallitis
-----look at HYPERAMMONEMIA in FA -- its causes cerebral edema
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  #155  
Old 06-03-2016
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Correct Answer

Quote:
Originally Posted by ginseng plus View Post
A 5 year old boy is brought to the emergency department because of a 16 hour history of severe vomiting and increased sleepiness. His mother says that he had a flulike illness 5 days ago that she treated with aspirin. Shortly after admission, he becomes delirious and then comatose.... His prothrombin time is prolonged. Serum studies show increased ammonia and lactate concentration and increased transaminase activities. Which of the following is the most likely cause of this patients coma?

Cerebral edema
Metabolic alkalosis
Subarachnoid hemorrhage wronggggggggg
venous sinus thrombosis
viral encephallitis
-----look at HYPERAMMONEMIA in FA -- it causes cerebral edema
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  #156  
Old 06-10-2016
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Info Nbme 16

Quote:
Originally Posted by ginseng plus View Post
It's very important tu understand in every NBME what they want from us to know

It's a classic features of gigantism, enlarged nose, hands, feet.
Occur in adult people, problem is with increased Growth hormone secretion,
I'am not discovering here nothing new, just try to analyze some quetions...

Insulin like peptide is increased, which work through tyrosine kinase receptor.
I chose tyrosine kinase and it was wrong ... I guess its A ... Adenyl cyclase since he is talking about Gs late in the question
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  #157  
Old 01-16-2017
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[QUOTE=ginseng plus;573497]Immunology

A 54 yo woman who works as a nurse comes to the physician for routine tuberculosis screening. A sample of her whole blood is incubated within a mixture of the synthetic peptides representing two proteins of the suspected pathogen. Three days later. supernatant is collected for evaluation. Measurement of which of the following cytokine concentration is most likely to indicate a positive result?

Granulocyte macrophage colony stimulating factor
Interferon alpha
Interferon gamma
Interleuking 4
interleukin 10
Transforming growth factorr betta

is the answer inteferon gamma?
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  #158  
Old 01-21-2017
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Quote:
Originally Posted by ginseng plus View Post
A male newborn delivered at 28 weeks gestation is tachypneic and hypoxemic. Which of the following altered structure changes in the type 2 pneumocytes is the most likely cause of this patient's condition?

Abundant rought endoplasmic reticulum wrong
Decreased numbers of lamellar bodies
Distinct junctional complexes with adjacent type 1 pneumocytes
NUmerous microvilli
Reticular fibers


I would like to say that , all this i do for myself primarily, but if someone find interesting , you are welcome...

Prior 35 weeks of gestaion, newborn have deficient surfactant secretion...
Acute respiratory distress syndrome

May be caused by trauma , sepsis , shock, gastric aspiration, uremia ,a acute pancreatitis, or amniotic fluid embolism. Diffuse alveolar damage, INcrease alveolar permeability capilary, protein rich leakage into alveoli. Resaults in formation of intra-alveolar hyaline menmbrane.
Initial damage due to release of neutrophilic substances toxic to alveolar wall, activation of coagulation cascade, and oxygen derived free radicals,...


Microvilli aren't present on terminal alveoli

I think it is Distinct junctional complexes with adjacent type 1 pneumocytes

If someone have corect answer post please....

i guess it absence of lamellar bodies as lamellar bodies among type 2 pneumocytes secrete surfactant which is absent in NRDS
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