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  #1  
Old 12-01-2014
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Romania NBME 12 discussion !!!!!!!!!!!!!!!!!!!!!!

Hi, here i'll try again in a free time to discuss nbme 12 which is offline at this time, but don't want to escape some 200 quetions similar as content and concepts as USMLE real exam,,,

For forum members desire to be active...
Thanks
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  #2  
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Romania Hi

I'' try to answer, you just say that i'm corectly understand quetion...

Nuclear gene, because it is steroid hormone???
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  #3  
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Star Hi

Dislocation or subluxation???

They're easy to confuse. But a dislocated shoulder and a separated shoulder are two distinct injuries. Here's the rundown.

Dislocated shoulder. In this injury, a fall or blow causes the top of your arm bone to pop out of the shoulder socket. Unlike a lot of joints in your body -- your elbow, for instance -- the shoulder is incredibly mobile. You can twist and move your upper arm in almost any direction. But there's a price for this ease of movement. The shoulder joint is inherently unstable, prone to slipping out of place.
In severe cases of dislocated shoulder, the tissue and nerves around the shoulder joint get damaged. If you keep dislocating your shoulder, you could wind up with chronic instability and weakness.
Separated shoulder. Despite the name, this injury doesn't directly affect the shoulder joint. Instead, a fall or blow tears one of the ligaments that connects the collarbone to the shoulder blade.
Since it's no longer anchored, the collarbone may move out of position and push against the skin near the top of your shoulder. Although separated shoulders can cause deformity, people usually recover fully with time.
You might get a separated shoulder or a dislocated shoulder by:

Falling onto your shoulder, especially on a hard surface
Being hit in the shoulder
Trying to break a fall with your hand
Dislocated shoulders can also result from a sharp twisting of the arm.

Sports that pose a higher risk of these two injuries are:

Football
Hockey
Rock climbing
Rugby
Soccer
Skiing
Volleyball


What Does a Dislocated Shoulder or Separated Shoulder Feel Like?
Symptoms of a dislocated shoulder are:

Pain in the shoulder and upper arm that hurts more when you move the area
Deformation of the shoulder -- a bump in the front or back of your shoulder, depending on how the bone has been dislocated
Symptoms of a separated shoulder are:

Intense pain as soon as the injury occurs
Tenderness of the shoulder and collarbone
Swelling
Bruising
Deformed shoulder
To diagnose a separated shoulder or dislocated shoulder, your doctor will give you a thorough exam. You may need X-rays to rule out broken bones and other conditions
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  #4  
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Correct Answer

Quote:
Originally Posted by sashabeliimd View Post
I'' try to answer, you just say that i'm corectly understand quetion...

Nuclear gene, because it is steroid hormone???
Radial head subluxation,

also known as pulled elbow or nursemaid’s elbow, is the most common upper-extremity injury in infants and young children who present to the emergency department (ED). Reduction of the subluxed radial head is easily performed in the ED, and complications are rare.

Subluxation of the radial head is a minor soft tissue injury with a peak incidence in children aged 2-3 years and generally affecting children younger than 6 years.[1] Although occurrence outside this population is uncommon, radial head subluxation does occur in patients younger than 6 months, as well as in older children and even adults.[2]

Subluxation of the radial head typically results from a quick pull on a child’s arm (see the image below).[3] Often this occurs when a child is holding hands with a caregiver who lifts the child by the arm or tries to prevent a fall. Parents therefore may provide a history of a fall preceding the injury. Half the time, however, caregivers are unsure what caused the injury because the causative mechanical force can be minor or even trivial.[4] Rarely, underlying musculoskeletal abnormalities may precipitate a subluxation.[5]

Subluxation of radial head occurs after longitudin
Subluxation of radial head occurs after longitudinal traction is placed on pronated extended arm.
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Star

Behavioral quetion...
Boy have developmental delay, have a vocabulary in just 20 words, when at his age must know minimum 900 words.

Help please here to analyse quetion...
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Star Hi

Here answer is A, because have a blunt trauma, maybe spleen rupture with blood loss, and as compesatory mechanism will be increased heart rate, vasoconstriction in arteries and venules???
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  #7  
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Romania Hey guys please reply and help with this nbme

Behavioral

Face validity


From Wikipedia, the free encyclopedia
Face validity is the extent to which a test is subjectively viewed as covering the concept it purports to measure. It refers to the transparency or relevance of a test as it appears to test participants.[1][2] In other words, a test can be said to have face validity if it "looks like" it is going to measure what it is supposed to measure.[3] For instance, if you prepare a test to measure whether students can perform multiplication, and the people you show it to all agree that it looks like a good test of multiplication ability, you have shown the face validity of your test. Face validity is often contrasted with content validity and construct validity.

Some people use the term face validity only to refer to the validity of a test to observers who are not expert in testing methodologies. For instance, if you have a test that is designed to measure whether children are good spellers, and you ask their parents whether the test is a good test, you are studying the face validity of the test. If you ask an expert in testing spelling, some people would argue that you are not testing face validity.[4] This distinction seems too careful for most applications.[citation needed] Generally, face validity means that the test "looks like" it will work, as opposed to "has been shown to work".



External validity
From Wikipedia, the free encyclopedia
External validity is the validity of generalized (causal) inferences in scientific research, usually based on experiments as experimental validity.[1] In other words, it is the extent to which the results of a study can be generalized to other situations and to other people.[2] For example, inferences based on comparative psychotherapy studies often employ specific samples (e.g. volunteers, highly depressed, no comorbidity). If psychotherapy is found effective for these sample patients, will it also be effective for non-volunteers or the mildly depressed or patients with concurrent other disorders?

Situation: All situational specifics (e.g. treatment conditions, time, location, lighting, noise, treatment administration, investigator, timing, scope and extent of measurement, etc. etc.) of a study potentially limit generalizability.
Pre-test effects: If cause-effect relationships can only be found when pre-tests are carried out, then this also limits the generality of the findings.
Post-test effects: If cause-effect relationships can only be found when post-tests are carried out, then this also limits the generality of the findings.
Reactivity (placebo, novelty, and Hawthorne effects): If cause-effect relationships are found they might not be generalizable to other settings or situations if the effects found only occurred as an effect of studying the situation.
Rosenthal effects: Inferences about cause-consequence relationships may not be generalizable to other investigators or researchers.
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  #8  
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Romania Hi

i want to know that i'm clearly know and answer corectly nbme,

GnRH when is pulstile have a activating effect, and when is in continue secreted, inhibitind effect...

Which another answer matches better?
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  #9  
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Romania Smoking

Acute effects of cigarette smoking on cerebral oxygenation and hemodynamics: a combined study with near-infrared spectroscopy and transcranial Doppler sonography.

Terborg C1, Birkner T, Schack B, Witte OW.
Author information

Abstract

Cigarette smoking has been shown to increase cerebral blood flow velocity (CBFV) and reduce vasomotor reactivity temporarily. The aim of our study was to clarify whether this results from dilation of resistance vessels alone with subsequent increase in regional cerebral blood flow (rCBF), or an additional constriction of basal cerebral arteries. In 24 healthy smokers (mean age+/-S.D., 32.7+/-10.5 years), cerebral oxygenation and hemodynamics were monitored by transcranial Doppler sonography and near-infrared spectroscopy before, during, and after smoking a cigarette (nicotine 0.9 mg). We simultaneously recorded CBFV of both middle cerebral arteries, mean arterial blood pressure, skin blood flow, end-tidal CO(2), changes in concentration of cerebral oxyhemoglobin, deoxyhemoglobin, and total hemoglobin (micromol/l), and a cerebral tissue oxygenation index. Smoking increased CBFV (p<0.01), oxyhemoglobin (p<0.01), and total hemoglobin (p<0.01). After smoking, the increase in CBFV and total hemoglobin persisted (p<0.01), while oxyhemoglobin returned to baseline. Deoxyhemoglobin and cerebral tissue oxygenation index did not change during the whole procedure. During, but not after smoking, CBFV increase was correlated to ipsilateral changes in oxyhemoglobin and total hemoglobin (p<0.05). The increase in oxyhemoglobin only during smoking and the lack of changes in deoxyhemoglobin and cerebral tissue oxygenation index indicate that smoking did not substantially increase rCBF. The smoking-induced elevation in CBFV might therefore be due to an additional constriction of the middle cerebral artery. The combined effects of smoking on basal cerebral arteries and arterioles might contribute to the increased stroke risk in smokers.


Role of the locus coeruleus in the noradrenergic response to a systemic administration of nicotine.
Mitchell SN.
Author information
Abstract
Experiments were conducted using in vivo microdialysis to ascertain the role of nicotinic receptors in the terminal, or the cell body area, in the hippocampal noradrenaline response provoked by a systemic administration of nicotine.
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  #10  
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Romania Anemia

Patient with anemia, and in this case is problem with stomach, that may develop megaloblastic anemia, or if we see a decresed blood pressure i think is chronic bleeding, anemia of cronic silent hemorrhage.

Total number of erythrocytes and hemoglobin is decreased,
Answer will be decreased PaO2 ???
or some with decreased carrying capacity

Total O2 will decrease because number of carring cell, RBCs is decreased
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  #11  
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Romania Hi

Is anyone on life in this forum to help me with some quetions?
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Romania Hi

MOther statistics

Asked number needed to treat

Formula is 1/ arr

Please helpl and explane this table ....
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Default

Quote:
Originally Posted by sashabeliimd View Post
Patient with anemia, and in this case is problem with stomach, that may develop megaloblastic anemia, or if we see a decresed blood pressure i think is chronic bleeding, anemia of cronic silent hemorrhage.

Total number of erythrocytes and hemoglobin is decreased,
Answer will be decreased PaO2 ???
or some with decreased carrying capacity

Total O2 will decrease because number of carring cell, RBCs is decreased
The answer to this is decreased carrying capacity. So the total oxygen content will be decreased. This is straight out of FA. You can eliminate all the other answer choices because in anemia pao2 sao2 all stay the same.

And note: Try not to be so erratic/disorganized with your posts. and ppl might start responding to you.
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Thumbs Up Hi

Quote:
Originally Posted by 10blade View Post
The answer to this is decreased carrying capacity. So the total oxygen content will be decreased. This is straight out of FA. You can eliminate all the other answer choices because in anemia pao2 sao2 all stay the same.

And note: Try not to be so erratic/disorganized with your posts. and ppl might start responding to you.
Hey thanks for your reply, and sorry if it's looks some disorganized, but i want to analyse all them quickly fo course with members that are interested, and can help...
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Star Hi

Erlichiosis treatment
and mechanism of drug
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Correct Answer Hi

Quote:
Originally Posted by sashabeliimd View Post
Erlichiosis treatment
and mechanism of drug
Ehrlichia is a type of bacteria that infect dogs and other species worldwide, causing a disease called ehrlichiosis. Ehrlichiosis has also been called tropical canine pancytopenia (and several other names). Ehrlichia is commonly transmitted by ticks.

Cause
Ehrlichia bacteria infect white blood cells. There are many species of Ehrlichia, which infect a wide variety of animals, but there are only a few species that affect dogs. A closely related infection affecting platelets is caused by a bacteria called Anaplasma platys and is sometimes referred to as ehrlichiosis as well (Anaplasma platys used to be called Ehrlichia platys until recently).

Most Ehrlichia infections are acquired through tick bites. Infection is also possible via blood transfusions.

Risk Factors
Ehrlichiosis occurs worldwide in areas where the ticks that carry the disease are common. While any dog can be infected, some breeds, most notably German shepherds, are prone to more serious chronic infections.

Retired racing greyhounds from areas where ehrlichiosis is common may suffer from chronic, undetected infections and should be checked for ehrlichiosis and other tick-borne diseases when adopted.

Signs and Symptoms of Ehrlichiosis
The symptoms and severity of illness seen with ehrlichiosis depends on the species of Ehrlichia involved and the immune response of the dog. Generally, Erlichia canis appears to produce the most severe illness, and infections tend to progress through various stages.

The acute phase occurs within the first few weeks of being infected and is rarely fatal. Recovery can occur, or the dog can enter a "subclinical phase" which can last for years, where there are no symptoms. Some dogs, but not all, eventually progress to the chronic phase, where very severe illness can develop. However, in practice is is difficult to distinguish these phases.

Signs and symptoms of ehrlichiosis may include:

fever
lethargy
loss of appetite
weight loss
abnormal bleeding (e.g., nosebleeds, bleeding under skin -- looks like little spots or patches of bruising)
enlarged lymph nodes
enlarged spleen
pain and stiffness (due to arthritis and muscle pain)
coughing
discharge from the eyes and/or nose
vomiting and diarrhea
inflammation of the eye
neurological symptoms (e.g., incoordination, depression, paralysis, etc.)
Signs of other organ involvement can appear in the chronic form, especially kidney disease.


Note: Anaplasma platys causes recurrent low platelet counts but tends to produce only mild symptoms, if any.

Diagnosis of Ehrlichiosis
It can be difficult to confirm a diagnosis of ehrlichiosis. Blood tests typically show a decreased number of platelets ("thrombocytopenia") and sometimes decreased numbers of red blood cells (anemia) and/or white blood cells.

Changes in the protein levels in the blood may also occur. Blood smears can be examined for the presence of the Ehrlichia organisms. If they are present, the diagnosis can be confirmed, but they may not always show up on a smear. Blood can also be tested for antibodies to Ehrlichia, though this can sometimes produce incorrect results. Specialized testing can check for genetic material from Ehrlichia, and while this is the most sensitive test, it is not widely available and has some limitations as well. Generally, a combination of lab tests along with clinical signs and history are used to make a diagnosis.

The diagnosis is further complicated by the fact that dogs infected with Ehrlichia may also be infected with other diseases carried by ticks, such as Babesia, Lyme disease, or Rocky Mountain Spotted Fever. Infection with a bacteria called Bartonella has also been found in conjunction with Erlichiosis and other tick borne diseases.The presence of these other diseases can make symptoms more severe and and the diagnosis more complicated.

Treatment of Ehrlichiosis
Ehrlichiosis responds well to treatment with the anitbiotic doxycycline. Improvement in symptoms is usually very quick, but several weeks of treatment is usually needed to ensure a full recovery.

In severe cases where blood cell counts are very low, blood transfusions may be needed.

Reinfection is possible as immunity to Ehrlichia bacteria is not long lasting.

Prevention of Ehrlichiosis
Preventing exposure to the ticks that carry Ehrlichia is the best means of preventing ehrlichiosis. Check your dog daily for ticks and remove them as soon as possible (it is believed that ticks must feed for at least 24-48 hours to spread Ehrlichia). This is especially important in peak tick season or if your dog spends time in the woods or tall grass (consider avoiding these areas in tick season).

Products that prevent ticks such as monthly parasite preventatives (e.g., Frontline®, Revolution®) or tick collars (e.g., Preventic®) can be used; be sure to follow your veterinarian's advice when using these products. Keep grass and brush trimmed in your yard, and in areas where ticks are a serious problem, you may also consider treating the yard and kennel area for ticks.



Answer will be protein synthesis...
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  #17  
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Default Pregnancy

Mitral insuficiency???
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Post Hi

INtestinal occlusion???
but which is diagnosis?
Malrotation? http://www.ajronline.org/doi/full/10....179.6.1791429
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Default hi

Quote:
Originally Posted by sashabeliimd View Post
Mitral insuficiency???
its a normal response, she has volume overload, thats why the splitting, remember its normal in teenagers and pregnant women.
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Thumbs Up Hi

Quote:
Originally Posted by Coccidioda View Post
its a normal response, she has volume overload, thats why the splitting, remember its normal in teenagers and pregnant women.
Thank you very much , you again are in helping me with another couple of nbme quetions, please look at another, that a cannot find right one...
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  #21  
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Default NNT

Quote:
Originally Posted by sashabeliimd View Post
MOther statistics

Asked number needed to treat

Formula is 1/ arr

Please helpl and explane this table ....
Hi.. as you said, NNT= 1/ARR

ARR= event rate in control - event rate in Treatment
you just have to see which is which in this case they told you trace elements is control, so its 2.3% - 1.3 % = 1 since its in percen that will be = 0.1

at the end you just divide 1/0.1 = 100
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Default malrotation

Quote:
Originally Posted by sashabeliimd View Post
INtestinal occlusion???
but which is diagnosis?
Malrotation? http://www.ajronline.org/doi/full/10....179.6.1791429
Its malrotation, I honestly did it because i knew the other ones where not possible; there is air on the left side which could be caused by a volvulus due to the malrotation.
Hope this helps
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  #23  
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Default :)

Quote:
Originally Posted by sashabeliimd View Post
Acute effects of cigarette smoking on cerebral oxygenation and hemodynamics: a combined study with near-infrared spectroscopy and transcranial Doppler sonography.

Terborg C1, Birkner T, Schack B, Witte OW.
Author information

Abstract

Cigarette smoking has been shown to increase cerebral blood flow velocity (CBFV) and reduce vasomotor reactivity temporarily. The aim of our study was to clarify whether this results from dilation of resistance vessels alone with subsequent increase in regional cerebral blood flow (rCBF), or an additional constriction of basal cerebral arteries. In 24 healthy smokers (mean age+/-S.D., 32.7+/-10.5 years), cerebral oxygenation and hemodynamics were monitored by transcranial Doppler sonography and near-infrared spectroscopy before, during, and after smoking a cigarette (nicotine 0.9 mg). We simultaneously recorded CBFV of both middle cerebral arteries, mean arterial blood pressure, skin blood flow, end-tidal CO(2), changes in concentration of cerebral oxyhemoglobin, deoxyhemoglobin, and total hemoglobin (micromol/l), and a cerebral tissue oxygenation index. Smoking increased CBFV (p<0.01), oxyhemoglobin (p<0.01), and total hemoglobin (p<0.01). After smoking, the increase in CBFV and total hemoglobin persisted (p<0.01), while oxyhemoglobin returned to baseline. Deoxyhemoglobin and cerebral tissue oxygenation index did not change during the whole procedure. During, but not after smoking, CBFV increase was correlated to ipsilateral changes in oxyhemoglobin and total hemoglobin (p<0.05). The increase in oxyhemoglobin only during smoking and the lack of changes in deoxyhemoglobin and cerebral tissue oxygenation index indicate that smoking did not substantially increase rCBF. The smoking-induced elevation in CBFV might therefore be due to an additional constriction of the middle cerebral artery. The combined effects of smoking on basal cerebral arteries and arterioles might contribute to the increased stroke risk in smokers.


Role of the locus coeruleus in the noradrenergic response to a systemic administration of nicotine.
Mitchell SN.
Author information
Abstract
Experiments were conducted using in vivo microdialysis to ascertain the role of nicotinic receptors in the terminal, or the cell body area, in the hippocampal noradrenaline response provoked by a systemic administration of nicotine.

competitive inhibition, he has co2 poisoning
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  #24  
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Star Hi

Pneumococcal infection do not matches, because fever is absent,
Pneumoccal pneumonias is typical, not atypical...

Remain corect answer, bronchitis??? after some infection, maybe

Influenza virus, after flu?

Causes
By Mayo Clinic Staff
Acute bronchitis is usually caused by viruses, typically the same viruses that cause colds and flu (influenza). Antibiotics don't kill viruses, so this type of medication isn't useful in most cases of bronchitis.

The most common cause of chronic bronchitis is smoking cigarettes. Air pollution and dust or toxic gases in the environment or workplace also can contribute to the condition.
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  #25  
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Star Hi

Voice become hoarse...

I viewved in quetion some note about a mass placed superiorly to the lung, looks like Pancoast tumor, then answer will be with affecting of the sympathetic ganglion?
I know that recurent laryngeal nerve is responsible for voice...
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  #26  
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Star Hi

Quote:
Originally Posted by sashabeliimd View Post
Voice become hoarse...

I viewved in quetion some note about a mass placed superiorly to the lung, looks like Pancoast tumor, then answer will be with affecting of the sympathetic ganglion?
I know that recurent laryngeal nerve is responsible for voice...
A Pancoast tumor, also called a pulmonary sulcus tumor or superior sulcus tumor, is a tumor of the pulmonary apex. It is a type of lung cancer defined primarily by its location situated at the top end of either the right or left lung. It typically spreads to nearby tissues such as the ribs and vertebrae. Most Pancoast tumors are non-small cell cancers.

The growing tumor can cause compression of a brachiocephalic vein, subclavian artery, phrenic nerve, recurrent laryngeal nerve, vagus nerve, or, characteristically, compression of a sympathetic ganglion resulting in a range of symptoms known as Horner's syndrome.

Symptoms[edit]
Aside from cancer general symptoms such as malaise, fever, weight loss and fatigue, Pancoast tumour can include a complete Horner's syndrome in severe cases: miosis (constriction of the pupils), anhidrosis (lack of sweating), ptosis (drooping of the eyelid) and enophthalmos (sunken eyeball). In progressive cases, the brachial plexus is also affected, causing pain and weakness in the muscles of the arm and hand (thoracic outlet syndrome). The tumour can also compress the recurrent laryngeal nerve and from this a hoarse voice and bovine cough may occur.

In superior vena cava syndrome, obstruction of the superior vena cava by a tumour (mass effect) causes facial swelling cyanosis and dilatation of the veins of the head and neck.

A Pancoast tumor is an apical tumour that is typically found in conjunction with a smoking history. The clinical signs and symptoms can be confused with neurovascular compromise at the level of the superior thoracic aperture. The patient's smoking history, rapid onset of clinical signs and symptoms and pleuritic pain can suggest an apical tumour. A Pancoast tumor can give rise to both Pancoast syndrome and Horner's syndrome. When the brachial plexus roots are involved it will produce Pancoast syndrome; involvement of sympathetic fibres as they exit the cord at T1 and ascend to the superior cervical ganglion will produce Horner's syndrome.
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Star hey

Hey help here..
He have a increased in volume on palpation bladder, and is a result of lower blockage by benign prostatic hyperplasia???
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Default asthma

Quote:
Originally Posted by sashabeliimd View Post
Pneumococcal infection do not matches, because fever is absent,
Pneumoccal pneumonias is typical, not atypical...

Remain corect answer, bronchitis??? after some infection, maybe

Influenza virus, after flu?

Causes
By Mayo Clinic Staff
Acute bronchitis is usually caused by viruses, typically the same viruses that cause colds and flu (influenza). Antibiotics don't kill viruses, so this type of medication isn't useful in most cases of bronchitis.

The most common cause of chronic bronchitis is smoking cigarettes. Air pollution and dust or toxic gases in the environment or workplace also can contribute to the condition.
He has Asthma, check page 554 FA 2013, can be triggered by viral URI, wheezing and all symptoms are consistent
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Star Hi

Again quetion with relative risk

In statistics and epidemiology, relative risk (RR) is the ratio of the probability of an event occurring (for example, developing a disease, being injured) in an exposed group to the probability of the event occurring in a comparison, non-exposed group. Relative risk includes two important features: (i) a comparison of risk between two "exposures" puts risks in context, and (ii) "exposure" is ensured by having proper denominators for each group representing the exposure [1][2]


Answer is A, because only control groups are unexposed?
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Default correct

Quote:
Originally Posted by sashabeliimd View Post
Hey help here..
He have a increased in volume on palpation bladder, and is a result of lower blockage by benign prostatic hyperplasia???
yes he has BPH that is causing an obstruction, some patients can even present with delirium like in his case when its severe
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Star Hi

IN quetion is absent that, it'a a first of second born child, but from symptoms here is Rh incompatibility, that is manifested just in second pregnancy where merge a IgG synthesis to RBCs,...

In ABO hemolytic disease of the newborn (also known as ABO HDN) maternal IgG antibodies with specificity for the ABO blood group system pass through the placenta to the fetal circulation where they can cause hemolysis of fetal red blood cells which can lead to fetal anemia and HDN. In contrast to Rh disease, about half of the cases of ABO HDN occur in a firstborn baby and ABO HDN does not become more severe after further pregnancies.

Choice A with opsonization? C3b + IgG
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Star Nerve damage

Here is damaged nerve, i know that every muscle fiber have apart inervation from some branches of nerve, and if nerve is damaged, muscle can become atrophic,
Regeneration of peripheral nerves is made by wallerian way.
I think answer is with nerve regeneration...

Reply please
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Default hello

Quote:
Originally Posted by sashabeliimd View Post
IN quetion is absent that, it'a a first of second born child, but from symptoms here is Rh incompatibility, that is manifested just in second pregnancy where merge a IgG synthesis to RBCs,...

In ABO hemolytic disease of the newborn (also known as ABO HDN) maternal IgG antibodies with specificity for the ABO blood group system pass through the placenta to the fetal circulation where they can cause hemolysis of fetal red blood cells which can lead to fetal anemia and HDN. In contrast to Rh disease, about half of the cases of ABO HDN occur in a firstborn baby and ABO HDN does not become more severe after further pregnancies.

Choice A with opsonization? C3b + IgG
It will be the FC portion, because the one that crosses the placenta is IgG
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Thumbs Up Hi

Quote:
Originally Posted by Coccidioda View Post
It will be the FC portion, because the one that crosses the placenta is IgG
Ooh sure , thanks , Fc portion, is a portion of immunoglobulin, and in this case will be...
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Star Tinnitus

Tinnitus

is a common disorder with many possible causes. Most cases of tinnitus are subjective, but occasionally the tinnitus can be heard by an examiner. Otologic problems, especially hearing loss, are the most common causes of subjective tinnitus. Common causes of conductive hearing loss include external ear infection, cerumen impaction, and middle ear effusion. Sensorineural hearing loss may be caused by exposure to excessive loud noise, presbycusis, ototoxic medications, or Meniere's disease. Unilateral hearing loss plus tinnitus should increase suspicion for acoustic neuroma. Subjective tinnitus also may be caused by neurologic, metabolic, or psychogenic disorders. Objective tinnitus usually is caused by vascular abnormalities of the carotid artery or jugular venous systems. Initial evaluation of tinnitus should include a thorough history, head and neck examination, and audiometric testing to identify an underlying etiology. Unilateral or pulsatile tinnitus may be caused by more serious pathology and typically merits specialized audiometric testing and radiologic studies. In patients who are discomforted by tinnitus and have no remediable cause, auditory masking may provide some relief.


Here is infarct, and and zone affectet is right face to 4th ventricle
Dysmetria in right part of the body, than is affected contralateral LEFT ??? B
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Star Mean

Mean median mode,

All decrease???
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Default hey

Quote:
Originally Posted by sashabeliimd View Post
Tinnitus

is a common disorder with many possible causes. Most cases of tinnitus are subjective, but occasionally the tinnitus can be heard by an examiner. Otologic problems, especially hearing loss, are the most common causes of subjective tinnitus. Common causes of conductive hearing loss include external ear infection, cerumen impaction, and middle ear effusion. Sensorineural hearing loss may be caused by exposure to excessive loud noise, presbycusis, ototoxic medications, or Meniere's disease. Unilateral hearing loss plus tinnitus should increase suspicion for acoustic neuroma. Subjective tinnitus also may be caused by neurologic, metabolic, or psychogenic disorders. Objective tinnitus usually is caused by vascular abnormalities of the carotid artery or jugular venous systems. Initial evaluation of tinnitus should include a thorough history, head and neck examination, and audiometric testing to identify an underlying etiology. Unilateral or pulsatile tinnitus may be caused by more serious pathology and typically merits specialized audiometric testing and radiologic studies. In patients who are discomforted by tinnitus and have no remediable cause, auditory masking may provide some relief.


Here is infarct, and and zone affectet is right face to 4th ventricle
Dysmetria in right part of the body, than is affected contralateral LEFT ??? B
the answer will be the inferior cerebellar peduncle wich is labeled as A (ipsilateral).
if its not large enough acoustic neuromas will be in the cerebellopontine angle, but as they grow they can get to the inferior cerebellar peduncle.
hope this helps
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Hi everyone! Does anyone have goljan lectures for step 1 and step 2. I ll be grateful if somebody sends them to me.
Thanks
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Default mode

Quote:
Originally Posted by sashabeliimd View Post
Mean median mode,

All decrease???
The mode will not change, remember mode is the number that repeats the most, in both cases even if you delete the last one, 0.8 will still be the mode.
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Thumbs Up Hi

Quote:
Originally Posted by Coccidioda View Post
The mode will not change, remember mode is the number that repeats the most, in both cases even if you delete the last one, 0.8 will still be the mode.
Mean, median, and mode are three kinds of "averages". There are many "averages" in statistics, but these are, I think, the three most common, and are certainly the three you are most likely to encounter in your pre-statistics courses, if the topic comes up at all.

The "mean" is the "average" you're used to, where you add up all the numbers and then divide by the number of numbers. The "median" is the "middle" value in the list of numbers. To find the median, your numbers have to be listed in numerical order, so you may have to rewrite your list first. The "mode" is the value that occurs most often. If no number is repeated, then there is no mode for the list.

The "range" is just the difference between the largest and smallest values.

Find the mean, median, mode, and range for the following list of values:
13, 18, 13, 14, 13, 16, 14, 21, 13

The mean is the usual average, so:

(13 + 18 + 13 + 14 + 13 + 16 + 14 + 21 + 13) ÷ 9 = 15

Note that the mean isn't a value from the original list. This is a common result. You should not assume that your mean will be one of your original numbers.

The median is the middle value, so I'll have to rewrite the list in order:

13, 13, 13, 13, 14, 14, 16, 18, 21

There are nine numbers in the list, so the middle one will be the (9 + 1) ÷ 2 = 10 ÷ 2 = 5th number:

13, 13, 13, 13, 14, 14, 16, 18, 21

So the median is 14.

The mode is the number that is repeated more often than any other, so 13 is the mode.

The largest value in the list is 21, and the smallest is 13, so the range is 21 – 13 = 8.

mean: 15
median: 14
mode: 13
range: 8

IN quetion we have mean is 1.08
median is 1.0
mode is 0.8 because occur most often

If we will delete on last, ok i got it thanks again....


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A study is conducted of nerve regeneration after injury in an experimental animal. A nerve guidance conduit is placed within a 4mm gap of a severed nerve. The conduit, filled with a keratin gel extracted from human hair, if sound to enhance visible nerve regeneration across the gap. Microscopic examination of the regeneration site after initial exposure to the keratin gel would most likely show mitotic activity in which of the following cells?

a.) fibroblasts
b.) macrophages
c.) neurons
d.) plasma cells
e.) schwann cells
f.) undifferentiated stem cells
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Default

Quote:
Originally Posted by sashabeliimd View Post
A study is conducted of nerve regeneration after injury in an experimental animal. A nerve guidance conduit is placed within a 4mm gap of a severed nerve. The conduit, filled with a keratin gel extracted from human hair, if sound to enhance visible nerve regeneration across the gap. Microscopic examination of the regeneration site after initial exposure to the keratin gel would most likely show mitotic activity in which of the following cells?

a.) fibroblasts
b.) macrophages
c.) neurons
d.) plasma cells
e.) schwann cells
f.) undifferentiated stem cells


Keratin gel filler for peripheral nerve repair in a rodent sciatic nerve injury model.
Lin YC1, Ramadan M, Van Dyke M, Kokai LE, Philips BJ, Rubin JP, Marra KG.
Author information
Abstract
BACKGROUND:
Restoration with sufficient functional recovery after long-gap peripheral nerve damage remains a clinical challenge. In vitro, keratins, which are derived from human hair, enhance activity and gene expression of Schwann cells. The specific aim of the authors' study was to examine keratin gel as conduit filler for peripheral nerve regeneration in a rat sciatic nerve injury model.
METHODS:
Incorporation of glial cell line-derived, neurotrophic factor, double-walled microspheres into polycaprolactone nerve guides has demonstrated an off-the-shelf product alternative to promote nerve regeneration, and this conduit was filled with keratin gel and examined in a rat 15-mm sciatic nerve defect model. As an indicator of recovery, nerve sections were stained with S100 and protein gene product 9.5 antibody.
RESULTS:
The keratin-treated groups, compared with both saline and empty polycaprolactone (control) groups (p < 0.05), demonstrated a significantly increased density of Schwann cells and axons. Polycaprolactone-based nerve conduits possess optimal mechanical and degradative properties, rendering the biocompatible conduits potentially useful in peripheral nerve repair.
CONCLUSION:
From their studies, the authors conclude that polycaprolactone nerve guides with glial cell line-derived, neurotrophic factor-loaded, double-walled microspheres filled with keratin gel represent a potentially viable guiding material for Schwann cell and axon migration and proliferation in the treatment of peripheral nerve regeneration.


As viable material for schwann cell serve this keratin gel...
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2. A 25-year-old man is lost in the desert for 1 week with an ample supply of water but no food. Which of the following changes in enzyme activities and regulatory molecule concentrations in liver is most likely in this patient?

*fructose 2,6-bisphosphate *Glucose 6-phosphatase *PEPCK *pyruvate kinase

a.) increase, increase increase decrease
b.) increase, increase, decrease, decrease
c.) increase, decrease, decrease, increase
d.) decrease, increase, increase, decrease
e.) decrease, increase, decrease, decrease
f.) decrease, decrease, increase, increase
g.) decrease, decrease, decrease, increase
h.) decrease, decrease, decrease, decrease
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Post Hi

Quote:
Originally Posted by sashabeliimd View Post
2. A 25-year-old man is lost in the desert for 1 week with an ample supply of water but no food. Which of the following changes in enzyme activities and regulatory molecule concentrations in liver is most likely in this patient?

*fructose 2,6-bisphosphate *Glucose 6-phosphatase *PEPCK *pyruvate kinase

a.) increase, increase increase decrease
b.) increase, increase, decrease, decrease
c.) increase, decrease, decrease, increase
d.) decrease, increase, increase, decrease
e.) decrease, increase, decrease, decrease
f.) decrease, decrease, increase, increase
g.) decrease, decrease, decrease, increase
h.) decrease, decrease, decrease, decrease

Enzymes implicated in Gluconeogenesis:

Pyruvate carboxylase VS in glucolysis puruvate kinase
PEP carboxylase
Fructose.1.6Bpase
Glucose 6 phosphatase VS in glycolysis fructose2,6biphosphate
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Q3)
A 14-year-old boy is brought to the physician's office because of decreased appetite and abdominal pain over the past 3 weeks. His mother says that during the same time he has withdrawn from everyone and sleeps constantly. He describes his symptoms vaguely. Physical examination is normal. During further history-taking, it is most critical for the physician to obtain information about which of the following?

A
)
Developmental history

B
)
Family history of affective disorders

C
)
Orientation to time, place, and person

D
)
School history

E
)
Suicidal ideation or attempts
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Quote:
Originally Posted by sashabeliimd View Post
Q3)
A 14-year-old boy is brought to the physician's office because of decreased appetite and abdominal pain over the past 3 weeks. His mother says that during the same time he has withdrawn from everyone and sleeps constantly. He describes his symptoms vaguely. Physical examination is normal. During further history-taking, it is most critical for the physician to obtain information about which of the following?

A
)
Developmental history

B
)
Family history of affective disorders

C
)
Orientation to time, place, and person

D
)
School history

E
)
Suicidal ideation or attempts
It'a depression major, or maybe atypical becase sleep more time than before...
Suicidal ideas , may come to person....
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Romania Hi

. A 79 years old women with osteoarthritis comes to the physician for an initial examaniton. She is otherwise healthy and lives alone. When the physician enters the examination room he detects a slight odour suggestive of urine, it is most appropriate for the physician to approach the topics of urinary incontinence with this patient with which of the following way.

a. Are u having any problem that u may be too embarrassed to talk about? Would u be willing to talk about them today. (wrong)

b. I couldn’t help but noticed a odor when I entered the room. Are u having any difficulties in having holding ur urine.

c. I understand this can difficult to talk about but do u also finds urself having fecal incontinence in addition to urinary incontinence.

d. I know this can be an embarrassing topics but ppl sometimes have difficulties in holding their urine as they get older. Is this ever a problem for u.>>>>>>>>>>>>>>>>>>>>>

e. It is not surprising that some1 at ur age having difficulties holding urine. How many accidents u have in a day.



Direct quetions to patient to problem that exist... Avoid judgmental terms.
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Default depression

Quote:
Originally Posted by sashabeliimd View Post
It'a depression major, or maybe atypical becase sleep more time than before...
Suicidal ideas , may come to person....
Suicidal Ideations is the answer
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Post Hi

A 35-year-old woman with HIV infection has a first generalized tonic-clonic seizure. An MRI shows a small, solitary, enhancing lesion in the right frontal lobe. If stereotactic biopsy of this lesion were performed, it would show intense infiltration of lymphocytes, plasma cells, and macrophages and numerous 3 x 7-mm crescent-shaped organisms with central nuclei. The lesion regresses slowly after treatment with sulfonamide and pyrimethamine. Which of the following is the most likely mode of transmission of this infection?

A) Blood transfusion
B) Ingestion
C) Migration across cribiform plate
D) Sexual intercourse
E) Small droplet inhalation - not the answer
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Default :)

Quote:
Originally Posted by sashabeliimd View Post
. A 79 years old women with osteoarthritis comes to the physician for an initial examaniton. She is otherwise healthy and lives alone. When the physician enters the examination room he detects a slight odour suggestive of urine, it is most appropriate for the physician to approach the topics of urinary incontinence with this patient with which of the following way.

a. Are u having any problem that u may be too embarrassed to talk about? Would u be willing to talk about them today. (wrong)

b. I couldn’t help but noticed a odor when I entered the room. Are u having any difficulties in having holding ur urine.

c. I understand this can difficult to talk about but do u also finds urself having fecal incontinence in addition to urinary incontinence.

d. I know this can be an embarrassing topics but ppl sometimes have difficulties in holding their urine as they get older. Is this ever a problem for u.>>>>>>>>>>>>>>>>>>>>>


e. It is not surprising that some1 at ur age having difficulties holding urine. How many accidents u have in a day.



Direct quetions to patient to problem that exist... Avoid judgmental terms.
D is the answer
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Romania

Quote:
Originally Posted by sashabeliimd View Post
A 35-year-old woman with HIV infection has a first generalized tonic-clonic seizure. An MRI shows a small, solitary, enhancing lesion in the right frontal lobe. If stereotactic biopsy of this lesion were performed, it would show intense infiltration of lymphocytes, plasma cells, and macrophages and numerous 3 x 7-mm crescent-shaped organisms with central nuclei. The lesion regresses slowly after treatment with sulfonamide and pyrimethamine. Which of the following is the most likely mode of transmission of this infection?

A) Blood transfusion
B) Ingestion >>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>
C) Migration across cribiform plate nooooo
D) Sexual intercourse
E) Small droplet inhalation - not the answer

Toxoplasma gondii: from animals to humans.
Tenter AM1, Heckeroth AR, Weiss LM.
Author information
Erratum in
Int J Parasitol 2001 Feb;31(2):217-20.
Abstract
Toxoplasmosis is one of the more common parasitic zoonoses world-wide. Its causative agent, Toxoplasma gondii, is a facultatively heteroxenous, polyxenous protozoon that has developed several potential routes of transmission within and between different host species. If first contracted during pregnancy, T. gondii may be transmitted vertically by tachyzoites that are passed to the foetus via the placenta. Horizontal transmission of T. gondii may involve three life-cycle stages, i.e. ingesting infectious oocysts from the environment or ingesting tissue cysts or tachyzoites which are contained in meat or primary offal (viscera) of many different animals. Transmission may also occur via tachyzoites contained in blood products, tissue transplants, or unpasteurised milk. However, it is not known which of these routes is more important epidemiologically. In the past, the consumption of raw or undercooked meat, in particular of pigs and sheep, has been regarded as a major route of transmission to humans. However, recent studies showed that the prevalence of T. gondii in meat-producing animals decreased considerably over the past 20 years in areas with intensive farm management. For example, in several countries of the European Union prevalences of T. gondii in fattening pigs are now <1%. Considering these data it is unlikely that pork is still a major source of infection for humans in these countries. However, it is likely that the major routes of transmission are different in human populations with differences in culture and eating habits. In the Americas, recent outbreaks of acute toxoplasmosis in humans have been associated with oocyst contamination of the environment. Therefore, future epidemiological studies on T. gondii infections should consider the role of oocysts as potential sources of infection for humans, and methods to monitor these are currently being developed. This review presents recent epidemiological data on T. gondii, hypotheses on the major routes of transmission to humans in different populations, and preventive measures that may reduce the risk of contracting a primary infection during pregnancy.
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Default T. gondii

Quote:
Originally Posted by sashabeliimd View Post
A 35-year-old woman with HIV infection has a first generalized tonic-clonic seizure. An MRI shows a small, solitary, enhancing lesion in the right frontal lobe. If stereotactic biopsy of this lesion were performed, it would show intense infiltration of lymphocytes, plasma cells, and macrophages and numerous 3 x 7-mm crescent-shaped organisms with central nuclei. The lesion regresses slowly after treatment with sulfonamide and pyrimethamine. Which of the following is the most likely mode of transmission of this infection?

A) Blood transfusion
B) Ingestion
C) Migration across cribiform plate
D) Sexual intercourse
E) Small droplet inhalation - not the answer
patient clearly has toxoplasma gondii, you just have to remember the route of transmission, (cyst in meat or oocytes in cat feces) both are by ingestion.
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26. A 45-year-old woman with multiple sclerosis is brought to the emergency department by a friend because of a 1-hour history of increasing confusion; she is now
stuporous. She has been in remission for 2 years. Her temperature is 37.2'C (99“F), pulse is 72/min, respirations are 8/min, and blood pressure is 116/66 mm Hg.
Percussion of the chest shows decreased lung volumes. The lungs are clear to auscultation. Breath sounds are distant There is a minimal gag response. When
amused, she is mildly combative, moves all four extremities, and then drift back into stupor. Arterial blood gas analysis on room air shows:

pH 7.12
Paco2 76 mm Hg
Po2 50 mm Hg


Which of the following is the most likely muse of this patients condition?

A) Acute respiratory distress syndrome
B) Aspiration pneumonia
C) opioid overdose
D) Pulmonary embolism
E) Upper airway obstruction
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Quote:
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26. A 45-year-old woman with multiple sclerosis is brought to the emergency department by a friend because of a 1-hour history of increasing confusion; she is now
stuporous. She has been in remission for 2 years. Her temperature is 37.2'C (99“F), pulse is 72/min, respirations are 8/min, and blood pressure is 116/66 mm Hg.
Percussion of the chest shows decreased lung volumes. The lungs are clear to auscultation. Breath sounds are distant There is a minimal gag response. When
amused, she is mildly combative, moves all four extremities, and then drift back into stupor. Arterial blood gas analysis on room air shows:

pH 7.12
Paco2 76 mm Hg
Po2 50 mm Hg


Which of the following is the most likely muse of this patients condition?

A) Acute respiratory distress syndrome
B) Aspiration pneumonia
C) opioid overdose >>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>
D) Pulmonary embolism
E) Upper airway obstruction
Respiratory depression OPIODS
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40. A 33-year-old man is brought to the emergency department 2 hours after injuring his left ankle while skiing. Examination of the left ankle shows swelling and exquisite
tenderness. An x-ray shows no abnormalities. A nonsteroidal anti-inflammatory drug (NSAIO) is prescribed. After his symptoms resolve and the patient stops taking
the NSAIO, the agent continues to have a prolonged effect on his platelet aggregation. Which of the fo llowing NSAIOs was most likely prescribed?
o A) Aspirin
o B) Celecoxib
o C) Oiclofenac
o 0 ) Ibuprofen
o E) Indomethacin
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Originally Posted by sashabeliimd View Post
40. A 33-year-old man is brought to the emergency department 2 hours after injuring his left ankle while skiing. Examination of the left ankle shows swelling and exquisite
tenderness. An x-ray shows no abnormalities. A nonsteroidal anti-inflammatory drug (NSAIO) is prescribed. After his symptoms resolve and the patient stops taking
the NSAIO, the agent continues to have a prolonged effect on his platelet aggregation. Which of the fo llowing NSAIOs was most likely prescribed?
o A) Aspirin
o B) Celecoxib
o C) Oiclofenac
o 0 ) Ibuprofen
o E) Indomethacin

Celecoxib, can be used, because escape COX 1 effect on stomach mucosa, but still have effect on COX2 which is selective and decrease synthesis of thromboxanes
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Romania Hi

) Healthy 6-month-old boy brought to physician b/c of a cough for 1 week. Initially he had a low-grade fever, sneezing, congestion, and runny nose. Then he develops a dry intermittent cough. The baby chokes and gasps if startled. No immunizations. Has paroxysms of "machine gun" like coughing with a forced expiratory grunt at the end of coughing. Leukocyte count is 30,000 (70% lymph). Neturophil chemotaxis and oxidative metabolism are defective due to increased activity of which?:

Adenylyl cyclase,
Myeloperoxidase, wrong
NADPH Oxidase,
Phospholipase C (wrong),
Protein Kinase C wrong

Whooping cough, clasical presentation of bordetella pertusis

Overactivates adenylate cyclase, by disabling Gi, impairing phagocytosis to permit survival of microbe.

Child choughs on expiration and whoops on inspiration..
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45 yo man has severe, substernal, crushing chest pain for the past 2 hours. His pulse is 100/min, respirations are 14/min, and blood pressure is 170/100 mmHg. A grade 3/6 holosystolic murmur is heard best over the cardiac apex. After treatment with oxygen, aspirin, nitroglycerin,morphine, and a thrombolytic, the chest pain resolves, and his blood pressure decreases to 120/60mmHg. Repeat auscultation of the chest does not detect a cardiac murmur.

Which of the following is the most likely cause of the murmur?

A: Acute aortic valve insufficiency wronggggg
B: aortic dissection wronggggg
C: atrial septal defect
D: Papillary muscle ischemia >>>>>>>>>>>>>>>>>>
E: Patent Ductus arteriosus wrong
F: Ventricular Septal Defect (wrong)
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Romania

Quote:
Originally Posted by sashabeliimd View Post
45 yo man has severe, substernal, crushing chest pain for the past 2 hours. His pulse is 100/min, respirations are 14/min, and blood pressure is 170/100 mmHg. A grade 3/6 holosystolic murmur is heard best over the cardiac apex. After treatment with oxygen, aspirin, nitroglycerin,morphine, and a thrombolytic, the chest pain resolves, and his blood pressure decreases to 120/60mmHg. Repeat auscultation of the chest does not detect a cardiac murmur.

Which of the following is the most likely cause of the murmur?

A: Acute aortic valve insufficiency wronggggg
B: aortic dissection wronggggg
C: atrial septal defect
D: Papillary muscle ischemia >>>>>>>>>>>>>>>>>>
E: Patent Ductus arteriosus wrong
F: Ventricular Septal Defect (wrong)

Ischemic mitral regurgitation (MR) is a complication of coronary heart disease; it primarily occurs in patients with a prior myocardial infarction (MI). MR may also occur with acute ischemia, a setting in which the MR typically resolves after the ischemia resolves. Following an MI, the MR is usually due to infarction with permanent damage to the papillary muscle or adjacent myocardium; in such patients, MR may become more severe with adverse remodeling of the left ventricle or subsequent ischemia. Thus, a better term for this condition might be “post-infarction” MR. (See "Mechanical complications of acute myocardial infarction".)

The optimal treatment of ischemic MR is a matter of controversy and there is wide variation in practice among cardiovascular surgeons. Much of this controversy stems from a lack of good data addressing this issue. There has been one randomized trial comparing mitral valve repair and replacement in this population [1]. Many of the early surgical studies included patients with different types of mitral valve disease, including patients who had degenerative mitral valve disease with prolapse and/or partial flail leaflet in association with coronary heart disease.

Better definitions of ischemic MR have evolved, as echocardiographic techniques have allowed appropriate classification of these patients. This has allowed the performance of higher quality studies, although the lack of randomized trials still limits the ability to make strong recommendations for management.

An overview of the presentation and management of patients with ischemic MR is presented here. The special case of papillary muscle rupture in the setting of acute MI is discussed briefly, but a more extensive review is found separately. (See "Mechanical complications of acute myocardial infarction".)


There are three major mechanical complications of acute myocardial infarction (MI): rupture of the left ventricular free wall; rupture of the interventricular septum; and the development of mitral regurgitation. One study compared 225 patients who had a first MI and experienced one of these complications to 1012 patients with a first MI without these mechanical complications [1]. Delayed hospitalization (≥24 hours), undue in-hospital physical activity, and postinfarction angina increased the risk of rupture in predisposed patients.

The clinical issues related to these mechanical problems, each of which can result in cardiogenic shock, will be reviewed here. (See "Clinical manifestations and diagnosis of cardiogenic shock in acute myocardial infarction".)

The 2004 American College of Cardiology/American Heart Association (ACC/AHA) guidelines on ST elevation MI and on coronary artery bypass graft surgery (CABG) recommended emergent surgery, with CABG if indicated, for these mechanical complications of an acute MI [2,3]. No changes to this approach were made in the 2007 ACC/AHA focused update [4].

In this topic MI will refer to ST elevation MI (STEMI), unless otherwise indicated
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A 52-year-old man with lung cancer comes to the physician for a follow-up examination. Smoking cessation has been recommended, but the patient says that he is unable to quit because he experiences a pleasurable sensation as he inhales the smoke. He has smoked 2 packs of cigarettes daily for 30 years. Which of the following mechanisms best explains how nicotine produces this sensation leading to addiction in this patient?

A)Activation of opioid receptors in the midbrain

B)Increased release of dopamine in the nucleus accumbens

C)Inhibition of γ-aminobutyric acid (GABA) release in the hypothalamus

D)Inhibition of glutamate receptors in the amygdala

E)Potentiation of GABA receptors in the cerebral cortex
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A 52-year-old man with lung cancer comes to the physician for a follow-up examination. Smoking cessation has been recommended, but the patient says that he is unable to quit because he experiences a pleasurable sensation as he inhales the smoke. He has smoked 2 packs of cigarettes daily for 30 years. Which of the following mechanisms best explains how nicotine produces this sensation leading to addiction in this patient?

A)Activation of opioid receptors in the midbrain

B)Increased release of dopamine in the nucleus accumbens

C)Inhibition of γ-aminobutyric acid (GABA) release in the hypothalamus

D)Inhibition of glutamate receptors in the amygdala

E)Potentiation of GABA receptors in the cerebral cortex

Recent research has shown how nicotine acts on the brain. Nicotine activates the circuitry that regulates feelings of pleasure, the so-called reward pathways. Research has shown that nicotine increases the levels of dopamine (a key brain chemical involved in mediating the desire to consume drugs) in the reward circuits. Nicotine's pharmacokinetic properties have been found to enhance its abuse potential. Cigarette smoking produces a rapid distribution of nicotine to the brain, with drug levels peaking within 10 seconds of inhalation. The acute effects of nicotine dissipate within a few minutes, causing the need to continue repeated intake throughout the day.

http://www.psychologytoday.com/conditions/nicotine
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Star Hi

i'm between answer where self induced vomiting, because weight loss, and restrictive calories, which is corect????
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A 32-year-old woman undergoes a laparoscopic cholecystectomy after ultrasonography showed a thickened gallbladder wall and gallstones. The surgeon will be unable to
inspect directly which of the following organs during this procedure?
o A) Ileum
o B) Jejunum
o C) Pancreas
o D) Stomach
o E) Transverse colon
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A 32-year-old woman undergoes a laparoscopic cholecystectomy after ultrasonography showed a thickened gallbladder wall and gallstones. The surgeon will be unable to
inspect directly which of the following organs during this procedure?
o A) Ileum
o B) Jejunum
o C) Pancreas
o D) Stomach
o E) Transverse colon
Pancreas is retroperitoneal, except tail part...
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Correct Answer Hi

Stroke Anticoagulation and Prophylaxis
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Stroke Anticoagulation and Prophylaxis
Practice Essentials
The role of anticoagulation in the treatment of cerebral ischemia has changed. For many years, it was used routinely in acute ischemic stroke. However, more current studies are helping to refine its role in the acute treatment and prevention of stroke. In addition, several new oral and parenteral anticoagulants are in different stages of clinical trials for use in the prophylaxis of ischemic thromboembolic stroke.

Anticoagulation for acute ischemic stroke
Current data do not support routine use of anticoagulation for acute ischemic stroke. However, anticoagulation continues to be recommended for some specific clinical situations. Indications currently proposed by many experts for early full-dose IV heparin after stroke or transient ischemic attack (TIA) include the following:

Conditions with potential high risk of early cardiogenic reembolization
Symptomatic dissection of the arteries supplying the brain
Symptomatic extracranial or intracranial arteriosclerotic stenosis with crescendo TIAs or early progressive stroke
Basilar artery occlusion before or after intra-arterial pharmacological or mechanical thrombolysis.
Known hypercoagulable states
Cerebral venous sinus thrombosis
Stroke prevention in atrial fibrillation
Oral anticoagulation is the therapy of choice for primary and secondary stroke prevention in patients with atrial fibrillation and any of the known additional risk factors.[1, 2] Asymptomatic patients younger than 65 years with atrial fibrillation and none of the other risk factors are at a low risk and either should be treated with aspirin or should not be treated at all.

Risk factors for bleeding
Risk factors for bleeding in anticoagulated patients include the following:

Hepatic or renal disease
Ethanol abuse
Malignancy
Old age (>75 years)
Rebleeding
Reduced platelet counts or platelet dysfunction
Hypertension that is uncontrolled
Anemia
Genetic factors
Elevated fall risk
Stroke
Stroke prevention after acute myocardial infarction
Anticoagulation for primary stroke prevention after myocardial infarction (MI) is recommended in patients with the following risk factors[3] :

Persistent or paroxysmal atrial fibrillation
Left ventricular thrombus
Left ventricular aneurysm
Extensive wall motion abnormalities resulting in a left ventricular ejection fraction (LVEF) < 25%
Stroke prevention in other heart diseases
Absolute indications for oral anticoagulation (primary and secondary stroke prevention) include the following:

Mechanical heart valve
Mitral valve stenosis with any prior embolic event
Left atrial myxoma (qualified support from the data)
Intraventricular thrombus
Ventricular aneurysm with thrombus
Mobile thrombus in the ascending
Dilated cardiomyopathy (qualified support from the data)
Oral anticoagulation is indicated for patients with a large patent foramen ovale (PFO) under 3 circumstances:

Recurrent cerebral ischemia while the patient was receiving aspirin, 300 mg/day
Co-occurrence of PFO with atrial septal aneurysm
Co-occurrence of PFO with deep venous thrombosis of the leg or abdomen
Other cardiac indications for oral anticoagulation for secondary stroke prevention include the following:

Mitral valve prolapse with myxomatous leaflets
Rupture of chordae tendineae
Dyskinetic ventricular wall segment
Mitral ring calcifications
No current evidence-based guidelines address anticoagulation in patients with symptomatic stenoses of extracranial and intracranial arteries.

Guidelines for secondary prevention

Class I recommendations from the American Heart Association/American Stroke Association (AHA/ASA) for prevention of stroke in patients who have experienced noncardioembolic ischemic stroke or TIA are as follows[4] :

Antiplatelet agents rather than oral anticoagulation are recommended to reduce the risk of recurrent stroke and other cardiovascular events (IA); aspirin monotherapy, the combination of aspirin and extended-release dipyridamole, and clopidogrel monotherapy are all acceptable options for initial therapy (IA)
For patients who have an ischemic cerebrovascular event while taking aspirin, increasing the dose of aspirin provides no additional benefit; the combination of aspirin and extended-release dipyridamole is recommended over aspirin alone (IB)

Class II recommendations are as follows:

Clopidogrel may be considered over aspirin alone (IIbB)
Clopidogrel is reasonable for patients allergic to aspirin (IIaB)
Class III recommendations are as follows:

Because of an increased risk of hemorrhage, combination therapy with aspirin and clopidogrel is not routinely recommended unless there is a specific indication for this therapy (IIIA)

In May 2013, new consensus guidelines on the delivery of optimized inpatient anticoagulation therapy were published.[5, 6] These guidelines, which were endorsed by the Anticoagulation Forum, call for the increased use of technology (eg, computerized physician order entry, bar code scanning, and dose range checking) for decreasing medication errors and increasing multidisciplinary involvement in the anticoagulation management system.[6]

Thrombophilia
In patients with cerebral ischemia of unknown origin who are younger than 40 years, a search for hereditary thrombophilia is generally recommended. Oral anticoagulation after cerebral ischemia is usually recommended for patients with the following disorders:

Antithrombin III deficiency
Protein C deficiency
Protein S deficiency
Activated protein C resistance
Plasminogen deficiency/inhibition
Dysfibrinogenemia
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A researcher wants to evaluate the association between asbestos exposure and mesothelioma. which of the following is the most appropriate study?

a)case control

b)case studies

c) ecologic

d) randomized clinical trial
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Quote:
Originally Posted by sashabeliimd View Post
A researcher wants to evaluate the association between asbestos exposure and mesothelioma. which of the following is the most appropriate study?

a)case control

b)case studies

c) ecologic

d) randomized clinical trial
Case control>>>>>>a group of people with the disease and compares them with a suitable comparison group without the disease...
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A 55-year-old woman is brought to the physician because of a 6-month-history of progressive difficulty walking. Neurologic examination shows spasticity, hyperreflexia, and clonus in the lower extremities. Babinski sign is present bilaterally. A drug with which of the following mechanisms of action will most likely decrease the spasticity in this patient?


A. Activation of γ-aminobutyric acid receptors in muscle spindle afferents (Is it this??)
B. Activation of glutamate receptors in gamma motoneurons (or this??)
C. Activation of serotonin receptors in alpha motoneurons
D. Inhibition of glycine receptors in Golgi tendon organ afferents
E. Inhibition of nicotinic receptors in Renshaw cells
F. Inhibition of α2 receptors in excitatory interneurons
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A 55-year-old woman is brought to the physician because of a 6-month-history of progressive difficulty walking. Neurologic examination shows spasticity, hyperreflexia, and clonus in the lower extremities. Babinski sign is present bilaterally. A drug with which of the following mechanisms of action will most likely decrease the spasticity in this patient?


A. Activation of γ-aminobutyric acid receptors in muscle spindle afferents (Is it this??)
B. Activation of glutamate receptors in gamma motoneurons (or this??)
C. Activation of serotonin receptors in alpha motoneurons
D. Inhibition of glycine receptors in Golgi tendon organ afferents
E. Inhibition of nicotinic receptors in Renshaw cells
F. Inhibition of α2 receptors in excitatory interneurons
Spasticity (from Greek spasmos-, meaning "drawing, pulling") is a feature of altered skeletal muscle performance with a combination of paralysis, increased tendon reflex activity and hypertonia. It is also colloquially referred to as an unusual "tightness", stiffness, or "pull" of muscles.

Clinically, spasticity results from the loss of inhibition of motor neurons, causing excessive muscle contraction. This ultimately leads to an hyperreflexia, an exaggerated deep tendon reflex. Spasticity is often treated with the drug baclofen, which acts as an agonist at GABA receptors, which are inhibitory and contribute to its efficacy as an antispasticity agent.

Spastic cerebral palsy is the most common form of cerebral palsy, which is group of permanent movement problems that do not get worse over time. GABA's inhibitory actions contribute to GABA's efficacy as an anti-spasticity agent.


Drug that decrease spasticity>>>>>>>> Baclofen
GABA agonist
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3 yr old boy,severe pain in right leg. Fracture right fibula,H/Obilateral gluteal maximus muscle weakness with 6 month history of intermittent pain in legs at night,cant keep up with others in playground.. best diagnostic tool

a. serum hydroxyproline
b.Serum Immunoglobulins
c.ESR
d. Rheumatoid factor
e.Creatine kinase activity.
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Romania Hi

Quote:
Originally Posted by sashabeliimd View Post
3 yr old boy,severe pain in right leg. Fracture right fibula,H/Obilateral gluteal maximus muscle weakness with 6 month history of intermittent pain in legs at night,cant keep up with others in playground.. best diagnostic tool

a. serum hydroxyproline
b.Serum Immunoglobulins
c.ESR
d. Rheumatoid factor
e.Creatine kinase activity.
Duchenne muscular dystrophy (DMD) is a recessive X-linked form of muscular dystrophy, affecting around 1 in 3,600 boys, which results in muscle degeneration and eventual death.[1] The disorder is caused by a mutation in the dystrophin gene, the largest gene located on the human X chromosome, which codes for the protein dystrophin, an important structural component within muscle tissue that provides structural stability to the dystroglycan complex (DGC) of the cell membrane. While both sexes can carry the mutation, females rarely exhibit signs of the disease.

Symptoms usually appear in male children before age 6 and may be visible in early infancy. Even though symptoms do not appear until early infancy, laboratory testing can identify children who carry the active mutation at birth.[2] Progressive proximal muscle weakness of the legs and pelvis associated with a loss of muscle mass is observed first. Eventually this weakness spreads to the arms, neck, and other areas. Early signs may include pseudohypertrophy (enlargement of calf and deltoid muscles), low endurance, and difficulties in standing unaided or inability to ascend staircases. As the condition progresses, muscle tissue experiences wasting and is eventually replaced by fat and fibrotic tissue (fibrosis). By age 10, braces may be required to aid in walking but most patients are wheelchair dependent by age 12. Later symptoms may include abnormal bone development that lead to skeletal deformities, including curvature of the spine. Due to progressive deterioration of muscle, loss of movement occurs, eventually leading to paralysis. Intellectual impairment may or may not be present but if present, does not progressively worsen as the child ages. The average life expectancy for individuals afflicted with DMD is around


The main symptom of Duchenne muscular dystrophy, a progressive neuromuscular disorder, is muscle weakness associated with muscle wasting with the voluntary muscles[citation needed] being first affected, especially affecting the muscles of the hips, pelvic area, thighs, shoulders, and calf muscles. Muscle weakness also occurs in the arms, neck, and other areas, but not as early as in the lower half of the body. Calves are often enlarged. Symptoms usually appear before age 6 and may appear as early as infancy. The other physical symptoms are:

Awkward manner of walking, stepping, or running. (patients tend to walk on their forefeet, because of an increased calf tonus. Also, toe walking is a compensatory adaptation to knee extensor weakness.)
Frequent falls
Fatigue
Difficulty with motor skills (running, hopping, jumping)
Increased Lumbar lordosis, leading to shortening of the hip-flexor muscles. This has an effect on overall posture and a manner of walking, stepping, or running.
Muscle contractures of achilles tendon and hamstrings impair functionality because the muscle fibers shorten and fibrosis occurs in connective tissue
Progressive difficulty walking
Muscle fiber deformities
Pseudohypertrophy (enlarging) of tongue and calf muscles. The muscle tissue is eventually replaced by fat and connective tissue, hence the term pseudohypertrophy.
Higher risk of neurobehavioral disorders (e.g., ADHD), learning disorders (dyslexia), and non-progressive weaknesses in specific cognitive skills (in particular short-term verbal memory), which are believed to be the result of absent or dysfunctional dystrophin in the brain.
Eventual loss of ability to walk (usually by the age of 12)
Skeletal deformities (including scoliosis in some cases)



Signs and tests

A positive Gowers' sign reflects the more severe impairment of the lower extremities muscles. The child helps himself to get up with upper extremities: first by rising to stand on his arms and knees, and then "walking" his hands up his legs to stand upright.
Affected children usually tire more easily and have less overall strength than their peers.
Creatine kinase (CPK-MM) levels in the bloodstream are extremely high.
An electromyography (EMG) shows that weakness is caused by destruction of muscle tissue rather than by damage to nerves.
Genetic testing can reveal genetic errors in the Xp21 gene.
A muscle biopsy (immunohistochemistry or immunoblotting) or genetic test (blood test) confirms the absence of dystrophin, although improvements in genetic testing often make this unnecessary.
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40 y/o woman comes in with joint pain, swelling of her PIP, wrist, knees, increased ESR with a normocytic normochromic anemia; serum is positive for rheumatoid factor, what would you see in the synovium?

Answers: All up/down arrows, with complement, segmented neutrophils, IL-1, TNF
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Quote:
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40 y/o woman comes in with joint pain, swelling of her PIP, wrist, knees, increased ESR with a normocytic normochromic anemia; serum is positive for rheumatoid factor, what would you see in the synovium?

Answers: All up/down arrows, with complement, segmented neutrophils, IL-1, TNF
Complement down, PMNs, IL1 and TNF up.

Blood tests

People with rheumatoid arthritis tend to have an elevated erythrocyte sedimentation rate (ESR, or sed rate), which indicates the presence of an inflammatory process in the body. Other common blood tests look for rheumatoid factor and anti-cyclic citrullinate d peptide (anti-CCP) antibodies

How do physicians diagnose rheumatoid arthritis?

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There is no singular test for diagnosing rheumatoid arthritis. The diagnosis is based on the clinical presentation. Ultimately, rheumatoid arthritis is diagnosed based on a combination of the presentation of the joints involved, characteristic joint swelling and stiffness in the morning, the presence of blood rheumatoid factor and citrulline antibody, as well as findings of rheumatoid nodules and radiographic changes (X-ray testing). It is important to understand that there are many forms of joint disease that can mimic rheumatoid arthritis.

The first step in the diagnosis of rheumatoid arthritis is a meeting between the doctor and the patient. The doctor reviews the history of symptoms, examines the joints for inflammation, tenderness, swelling, and deformity, the skin for rheumatoid nodules (firm bumps under the skin, most commonly over the elbows or fingers), and other parts of the body for inflammation. Certain blood and X-ray tests are often obtained. The diagnosis will be based on the pattern of symptoms, the distribution of the inflamed joints, and the blood and X-ray findings. Several visits may be necessary before the doctor can be certain of the diagnosis. A doctor with special training in arthritis and related diseases is called a rheumatologist.

It is the inflammation in the joint that helps to distinguish rheumatoid arthritis from common types of arthritis that are not inflammatory, such as osteoarthritis or degenerative arthritis. The distribution of joint inflammation is also important to the doctor in making a diagnosis. In rheumatoid arthritis, the small joints of the hands and fingers, wrists, feet, and knees are typically inflamed in a symmetrical distribution (affecting both sides of the body). When only one or two joints are inflamed, the diagnosis of rheumatoid arthritis becomes more difficult. The doctor may then perform other tests to exclude arthritis due to infection or gout. The detection of rheumatoid nodules (described above), most often around the elbows and fingers, can suggest the diagnosis.

Abnormal antibodies can be found in the blood of people with rheumatoid arthritis with simple blood testing. An antibody called "rheumatoid factor" (RF) can be found in 80% of patients with rheumatoid arthritis. Patients who are felt to have rheumatoid arthritis and do not have positive rheumatoid factor testing are referred to as having "seronegative rheumatoid arthritis." Citrulline antibody (also referred to as anticitrulline antibody, anticyclic citrullinated peptide antibody, and anti-CCP antibody) is present in 50%-75% people with rheumatoid arthritis. It is useful in the diagnosis of rheumatoid arthritis when evaluating cases of unexplained joint inflammation. A test for citrulline antibodies is especially helpful in looking for the cause of previously undiagnosed inflammatory arthritis when the traditional blood test for rheumatoid arthritis, rheumatoid factor, is not present. Citrulline antibodies have been felt to represent the earlier stages of rheumatoid arthritis in this setting. Citrulline antibodies also have been associated with more aggressive forms of rheumatoid arthritis. Another antibody called the "antinuclear antibody" (ANA) is also frequently found in people with rheumatoid arthritis.

A blood test called the sedimentation rate (sed rate) is a crude measure of the inflammation of the joints. The sed rate actually measures how fast red blood cells fall to the bottom of a test tube. The sed rate is usually faster (high) during disease flares and slower (low) during remissions. Another blood test that is used to measure the degree of inflammation present in the body is the C-reactive protein. Blood testing may also reveal anemia, since anemia is common in rheumatoid arthritis, particularly because of the chronic inflammation.

The rheumatoid factor, ANA, sed rate, and C-reactive protein tests can also be abnormal in other systemic autoimmune and inflammatory conditions. Therefore, abnormalities in these blood tests alone are not sufficient for a firm diagnosis of rheumatoid arthritis.

Joint X-rays may be normal or only demonstrate swelling of soft tissues early in the disease. As the disease progresses, X-rays can reveal bony erosions typical of rheumatoid arthritis in the joints. Joint X-rays can also be helpful in monitoring the progression of disease and joint damage over time. Bone scanning, a procedure using a small amount of a radioactive substance, can also be used to demonstrate the inflamed joints. MRI scanning can also be used to demonstrate joint damage.

The American College of Rheumatology has developed a system for classifying rheumatoid arthritis that is primarily based upon the X-ray appearance of the joints. This system helps medical professionals classify the severity of your rheumatoid arthritis with respect to cartilage, ligaments, and bone.

Stage I

No damage seen on X-rays, although there may be signs of bone thinning
Stage II

On X-ray, evidence of bone thinning around a joint with or without slight bone damage
Slight cartilage damage possible
Joint mobility may be limited; no joint deformities observed
Atrophy of adjacent muscle
Abnormalities of soft tissue around joint possible
Stage III

On X-ray, evidence of cartilage and bone damage and bone thinning around the joint
Joint deformity without permanent stiffening or fixation of the joint
Extensive muscle atrophy
Abnormalities of soft tissue around joint possible
Stage IV

On X-ray, evidence of cartilage and bone damage and osteoporosis around joint
Joint deformity with permanent fixation of the joint (referred to as ankylosis)
Extensive muscle atrophy
Abnormalities of soft tissue around joint possible
Rheumatologists also classify the functional status of people with rheumatoid arthritis as follows:

Class I: completely able to perform usual activities of daily living
Class II: able to perform usual self-care and work activities but limited in activities outside of work (such as playing sports, household chores)
Class III: able to perform usual self-care activities but limited in work and other activities
Class IV: limited in ability to perform usual self-care, work, and other activities
The doctor may elect to perform an office procedure called arthrocentesis. In this procedure, a sterile needle and syringe are used to drain joint fluid out of the joint for study in the laboratory. Analysis of the joint fluid in the laboratory can help to exclude other causes of arthritis, such as infection and gout. Arthrocentesis can also be helpful in relieving joint swelling and pain. Occasionally, cortisone medications are injected into the joint during the arthrocentesis in order to rapidly relieve joint inflammation and further reduce symptoms.


Complement component 3 (C3)Share on facebookShare on twitterBookmark & SharePrinter-friendly version
Complement C3 is a blood test that measures the activity of a certain protein that is part of the complement system. The complement system is a group of proteins that move freely through your bloodstream. The proteins work with your immune system and play a role in the development of inflammation.

There are nine major complement proteins. They are labeled C1 through C9. This test measures C3.

How the Test is Performed
Blood is drawn from a vein, usually from the inside of the elbow or the back of the hand. The site is cleaned with germ-killing medicine (antiseptic). The health care provider wraps an elastic band around the upper arm to apply pressure to the area and make the vein swell with blood.

Next, the health care provider gently inserts a needle into the vein. The blood collects into an airtight vial or tube attached to the needle. The elastic band is removed from your arm.

Once the blood has been collected, the needle is removed, and the puncture site is covered to stop any bleeding.

In infants or young children, a sharp tool called a lancet may be used to puncture the skin and make it bleed. The blood collects into a small glass tube called a pipette, or onto a slide or test strip. A bandage may be placed over the area if there is any bleeding.

How to Prepare for the Test
There is no special preparation needed.

How the Test Will Feel
When the needle is inserted to draw blood, some people feel moderate pain, while others feel only a prick or stinging sensation. Afterward, there may be some throbbing.

Why the Test is Performed
C3 and C4 are the most commonly measured complement components.

A complement test may be used to monitor patients with an autoimmune disorder and to see if treatment for their condition is working. For example, patients with active lupus erythematosus may have lower-than-normal levels of the complement proteins C3 and C4.

Complement activity varies throughout the body. For example, in patients with rheumatoid arthritis, complement activity in the blood may be normal or higher-than-normal, but much lower-than-normal in the joint fluid.

Additional conditions under which the test may be performed:

Fungal infections
Gram negative septicemia
Parasitic infections such as malaria
Paroxysmal nocturnal hemoglobinuria (PNH)
Shock
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  #75  
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a 56 year old woman comes to the physician 1 week after she noted that her skin and eyes were yellow. She has had an unintentional 9 kg (20 lb) weight loss during the past 4 months. Physical examination shows scleral icterus and mild epigastric tenderness on palpation. Lab studies show:

Hb 12g/dl
Hct 35%
Serum
total bilirubin 8 gm/dl
ALK Phosphatase 456 U/L

An abdominal CT scan shows a mass at the head of the pancreas. Which of the following procedures is most likely to relieve this patient's jaundice?

A) Cholecystectomy
B) Placement of a percutaneous stent into the hepatic duct
C) Placement of a stent into the common bile duct
D) Placement of a stent into the main pancreatic duct
E) placement of a stent percutaneously into the cystic duct
F) placement of a transjugular intrahepatic portosystemic shunt
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  #76  
Old 12-04-2014
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GIT

Quote:
Originally Posted by sashabeliimd View Post
a 56 year old woman comes to the physician 1 week after she noted that her skin and eyes were yellow. She has had an unintentional 9 kg (20 lb) weight loss during the past 4 months. Physical examination shows scleral icterus and mild epigastric tenderness on palpation. Lab studies show:

Hb 12g/dl
Hct 35%
Serum
total bilirubin 8 gm/dl
ALK Phosphatase 456 U/L

An abdominal CT scan shows a mass at the head of the pancreas. Which of the following procedures is most likely to relieve this patient's jaundice?

A) Cholecystectomy
B) Placement of a percutaneous stent into the hepatic duct
C) Placement of a stent into the common bile duct >>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>> >
D) Placement of a stent into the main pancreatic duct
E) placement of a stent percutaneously into the cystic duct
F) placement of a transjugular intrahepatic portosystemic shunt
Since the head of the pancreas is anatomically located next to the second and third parts of the duodenum, it obstructs the bile flow in the common bile duct. Therefore, a stent placed in the commmon bile duct would relieve the obstruction. Since the problem does not lie with the gallbladder, cholecystectomy or a stent placed in the cystic duct would not solve the problem. Similarly, placing a stent in the hepatic duct wouldn't solve the problem neither. Since bile doesn't flow through the main pancreatic duct, placing a stent there wouldn't improve this condition. Finally, TIPS is used for establishing venous flow, not bile flow (e.g. TIPS could be used in a patient who develops portal hypertension)
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Post Hi

3 month old boy with hypoglycemia, hypoketonemia, lactic acidosis, and hypercholesterolemia 4 hours after feeding; giving glucagon does not increase blood glucose and only worsens lactic acidosis by increasing lactate; what enzyme deficiency is this?

Answers: Fructose 1,6 bisphosphatase, Galactose 1 phosphate uridyltransferase, glucose-6-phosphatase, alpha 1,4 glucosidase, MCAD deficiency
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Correct Answer

Quote:
Originally Posted by sashabeliimd View Post
3 month old boy with hypoglycemia, hypoketonemia, lactic acidosis, and hypercholesterolemia 4 hours after feeding; giving glucagon does not increase blood glucose and only worsens lactic acidosis by increasing lactate; what enzyme deficiency is this?

Answers: Fructose 1,6 bisphosphatase, Galactose 1 phosphate uridyltransferase, glucose-6-phosphatase, alpha 1,4 glucosidase, MCAD deficiency
THE ENZYME glucose-6-phosphate dehydrogenase (G6PD) initiates the oxidative decarboxylation of glucose-6-phosphate in the pentose phosphate pathway. This reaction results in the regeneration of the coenzyme TPNH, and the formation of CO2 and pentose phosphate.

Since G6PD is present in most human tissues,1 the question whether abnormalities in glucose metabolism exist in patients with G6PD deficiency is raised.

Isotopic studies measuring the rate of glucose oxidation by the whole body from both glucose-1-C14 and glucose-6-C14 have demonstrated markedly diminished C14O2 in the expired air of G6PD deficient males.2

An abnormal oral glucose tolerance response in G6PD deficient subjects, suggesting a diabetic tendency, was reported by Chanmugam and Frumin.3 Pointing out that diabetic state is usually mild, occurring later in life, and may be relatively asymptomatic, these authors stated that it is still unknown whether similar results would be obtained with children possessing


http://archpedi.jamanetwork.com/arti...ticleid=501749
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  #79  
Old 12-04-2014
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Romania Hi

Hey guys i just finished doing NBME 12, think to be helpful with some review and explanation to test that i doing wrong, or just think that may help someone to understand better , and find a needed explanation quickly...
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