Morsetlis

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Lymphedema is due to blockage of the flow of lymph due to a resectioned lymph node.

The general flow of fluid is capillaries <-> interstitial <-> lymph. With a blockage of the lymph drainage, compression will help push lymph back into the interstitial, and then capillaries, where it can drain into other lymphatic systems that are thorough.

Diuretics act at the capillaries level and are therefore less effect than compression, not to mention that a person with lymphedema can be normovolemic and will then develop hypovolemia if you give them a diuretic.

Passive movement / exercise actually do treat lymphedema, but of course not as well as compression sleeves. If passive movement /exercise treated it entirely, it wouldn't be a problem in the first place.
 

Drteeth21

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Can someone explain to me this answer??

A 19 year old woman comes to the physician because of increasingly severe pain in the right hip during the past month. She has a 4 year old history of refractory inflammatory bowel disease with arthritis in the hands treated with corticosteroids for the past 2 years. An x ray of the pelvis shows collapse of the superior half of the rigth femoral head with preservation of the articular cartilage. The left hip appears normal. Which of the following is the most likely cause of the hip abnormality?
A) ankylosing Spondylitis
B) aseptic necrosis
C) gouty arthritis
D) multiple myeloma
E) septic arthritis

I put Ankylosing spondylitis because of the HLA association? anyone know what the right answer is??
 

frankyazz

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Can someone explain to me this answer??

A 19 year old woman comes to the physician because of increasingly severe pain in the right hip during the past month. She has a 4 year old history of refractory inflammatory bowel disease with arthritis in the hands treated with corticosteroids for the past 2 years. An x ray of the pelvis shows collapse of the superior half of the rigth femoral head with preservation of the articular cartilage. The left hip appears normal. Which of the following is the most likely cause of the hip abnormality?
A) ankylosing Spondylitis
B) aseptic necrosis
C) gouty arthritis
D) multiple myeloma
E) septic arthritis

I put Ankylosing spondylitis because of the HLA association? anyone know what the right answer is??
chronic corticosteroids = bad for bones = aseptic necrosis
 
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sanityonleave

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Can someone explain to me this answer??

A 19 year old woman comes to the physician because of increasingly severe pain in the right hip during the past month. She has a 4 year old history of refractory inflammatory bowel disease with arthritis in the hands treated with corticosteroids for the past 2 years. An x ray of the pelvis shows collapse of the superior half of the rigth femoral head with preservation of the articular cartilage. The left hip appears normal. Which of the following is the most likely cause of the hip abnormality?
A) ankylosing Spondylitis
B) aseptic necrosis
C) gouty arthritis
D) multiple myeloma
E) septic arthritis

I put Ankylosing spondylitis because of the HLA association? anyone know what the right answer is??
b) aseptic necrosis (aka avascular necrosis)

The x-ray presentation of collapse of the femoral head with preservation of the cartilage doesn't fit with AS. AS usually starts with the sacroiliac joint, though it can progress to the hip joint -- in the event that happens, it should lead to inflammation / pain / fusion (a more inflammatory picture with cartilage disruption and inflammation).

Collapse of the top half of the head without cartilaginous involvement describes a noninflammatory process -- aseptic (aka avascular) necrosis. This is likely due to her long-term corticosteroid use which is a very significant risk factor.

Even if it didn't necessarily include the x-ray findings and just said she had hip pain, I'd still point to necrosis from the steroids before AS (common things being common, after all) -- but with the x-ray findings that's a slam dunk.
 

Drteeth21

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oh good call guys. spot on that was dumb on my part.

Another Q

Can someone explain this
A previously healthy 40 year old man is brought to the emergency dept 1 hour after hte sudden onset of svre pain in his left leg while playing tennis. he has ruptured Achillese tendon and undergoes operative repair and long leg cast immobilization. six months later his calf is atrophied. whats tha most liklely cause of the decrease?
a) decreased glycogen synthesis
B) decreased myosin light chain phosphatase activity (wrong)
C) increased phosphatidyl degradation
D Increased protein degradation
E mito damage
E necrosis of muscle fibers
I saw myosin and just picked it but that operates smooth muscle so that was a dumb choice haha

and can someone explain WHY this answer is right
18 year old man has had temps, sore throat, cervical lymop hnode enlargment for 8 days. Latex agglutinatin pos for EBV. atypical cells with abundant lacey cytoplasm in the periph blood smear are most likely derived from which of the following cell types?
A) B cells (wrong)
B) basophils
C) neutrophils
D) plasma cells
E) T lymphocytes (why is this right>!)

9/10 times im putting B cells when I see EBV i have no idea why t cells would be right
 

ijn

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If you don't use your muscles then they atrophy by breaking down the myofibrils into their constitutive proteins. That protein is then shuttled into urea and gluconeogenesis.

Atypical (reactive) lymphocytes are T-cells. EBV does infect B-cells. I don't know why the T-cells become larger with certain viral infections.
 

Drteeth21

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ok cool thanks! so the first one should be protein degradation. how could you tel that theyre talking abut T cells over B cells though. B cells in mono would be atypical as well wouldnt they?
 

frankyazz

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EBV infects B cells. T cells kills other cells infected by viruses. The atypical lymphocyte is a T-cell reacting to the infected B cell. "Atypical" is not just a general term... it used to go by "Downey cell" and is supposed to represent the T-cell.
 

netminder

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b) aseptic necrosis (aka avascular necrosis)

The x-ray presentation of collapse of the femoral head with preservation of the cartilage doesn't fit with AS. AS usually starts with the sacroiliac joint, though it can progress to the hip joint -- in the event that happens, it should lead to inflammation / pain / fusion (a more inflammatory picture with cartilage disruption and inflammation).

Collapse of the top half of the head without cartilaginous involvement describes a noninflammatory process -- aseptic (aka avascular) necrosis. This is likely due to her long-term corticosteroid use which is a very significant risk factor.

Even if it didn't necessarily include the x-ray findings and just said she had hip pain, I'd still point to necrosis from the steroids before AS (common things being common, after all) -- but with the x-ray findings that's a slam dunk.
Corticosteroids inhibit osteoblast proliferation and differentiation directly. Glucocorticoids also increase bone resorption by decreasing secretion of androgens and estrogens, mediated primarily by inhibition of gonadotropin secretion. Also, glucocorticoids stimulate osteoclast proliferation by suppressing synthesis of osteoprotegerin, an inhibitor of osteoclast differentiation from the macrophage lineage, and by stimulating production of RANK, which is necessary for osteoclastogenesis. Glucocorticoids also induced stimulation of synthesis of RANKL by preosteoblasts/stromal cells, which supports osteoclast differentiation and net bone resorption.

Long answer. I'm thinking in this case with the osteonecrosis of the hip, the increase in bone resorption by decreasing secretion of sex steroids (along with the other factors above coming into play) probably contributes most significantly to inability of the bone (especially on the weight-bearing surface, as described in the question stem) to remodel following repetitive stress --> stress fractures --> don't heal on corticosteroids --> vicious cycle.

Butt-nasty test, this was.
 

sunyD

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Okay, am I missing something or is this one of those wtf questions?

A 55 yo man with hepatic encephalopathy is brought to the physician because of confusion and increased lethargy during the past 24 hrs. He has a history of cirrhosis of the liver caused by hepatitis C. He is easily a rousable despite the lethargy. His temp is 37. Physical examination shows scleral icterus, asterixis, a protuberant abdomen, and ascites. Test of the stool for occult blood is negative. Administration of which of the following drugs is most likely to improve this patient's mental status.

A. Bisacodyl
B. Docusate
C. Lactulose
D. Octreotide
E. Omeprazole
F. Sucralfate
G. Ursodiol
 

ijn

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Using lactulose to treat hepatic encephalopathy is pretty high yield. Definitely not a WTF question.
 

sunyD

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Good thing I asked then. Thanks.

I found it on page 4 of kaplan...I haven't checked that section in months since its pharmacokinetics...
 
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Hey all, here's a couple questions that I couldn't find a good answer for:

Section 1, #39
A 25 yo with cystic fibrosis comes in with a 3-day history of fever, cough, shortness of breath. His temp is 100.4 F and RR is 32. Bilateral crackles and rhonchi are heard. A culture grows aerobic, oxidase positive, gram negative rods that form slimy colonies and produce pyocyanin. It does not ferment lactose, treatment with multiple antibiotics hasn't worked. What is the best explanation for the persistent colonization of this patient?
A: bacteriophage superinfection
B: biofilm formation in the lower respiratory tract
C: overgrowth of acapsular strains
D: pyocyanin synthesis
E: synthesis of exotoxin A (wrong)

He's got pseudomonas, is it the biofilm?

Section 3, #6
A previously healthy 32 yo man comes in to the ER with a 1 day history of intermittent flashing spots/blurred vision, vomiting, confusions, and difficulty walking. He is painter and yesterday cleaned up a paint thinner spill. He has dilated pupils with hyperemia of the optic disc and retinal edema. He has tachypnea and an anion gap metabolic acidosis. The most appropriate therapy will inhibit the activity of which of the following?
A: alcohol dehydrogenase
B: aldehyde dehydrogenase
C: formaldehyde dehydrogenase (total guess, wrong)
D: lactate dehydrogenase
E: pyruvate dehydrogenase

Section 3, #36
A 54 yo woman with a 5 day history of severe mid-back pain. Exam shows point tenderness over T6 vertebrae. Serum calcium is 13.4 mg/dL, urinalysis shows Bence Jones proteins. What is the most likely cause of her hypercalcemia?
A: excessive PTH production
B: excessive PTHrP production
C: increased fractional calcium GI absorption
D: local IL-1 and tumor necrosis factor effects
E: unregulated 1,25 dihydroxycholecalciferol production (wrong)

So she's got multiple myeloma, what's the mechanism of hypercalcemia in MM? I thought it had something to do with elevated vitamin D.
 

ijn

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Hypercalcemia in sarcoidoisis is due to elevated 1,25 vitamin D. Multiple myeloma and other lytic bone cancers are due to increased IL-1/TNF alpha. Remember the other name for IL-1 is osteoclast activating factor.

I think the guy was poisoned by methanol. You should give ethanol or fompeizole to inhibit alcohol dehydrogenase to prevent the buildup of formaldehyde and subsequent formic acid.

The decreased mucociliary clearance in CF promotes biofilm formation and persistent reinfection. Exotoxin would explain any acute effects of the pseudomonas infection, but doesn't explain chronic colonization. Anytime you hear the words colonization in association with bacteria then think biofilm.
 
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Not sure if anyone agrees but I think 13 was way more of a ball breaker than 7. Many "are you a good test taker" questions with many "distractor in stem" questions in between. Just my 2c.
 

VisionaryTics

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Not sure if anyone agrees but I think 13 was way more of a ball breaker than 7. Many "are you a good test taker" questions with many "distractor in stem" questions in between. Just my 2c.
I took it yesterday, and that was my thought. All of the wtf questions were actually just simple concepts if you could pick apart the stem. I thought it was pretty straightforward as long as you didn't get hung up on their sttempts to confuse you.
 

netminder

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Azipropofol, I agree -- particularly with your assessment of the ball-breaking component. I didn't take NBME 7, but I did find NBME 13 to be moderately irritating.
 

tele turnin

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37.
A 5-year-old girl is brought to the physician because of listlessness, fatigue, and dull pain in the right upper quadrant of the abdomen. Her height and weight are below the 25th percentile. Laboratory findings indicate that the content of her &#946;-globin chain is 15% to 20% of normal. Sequencing of the &#946;-globin gene shows a point mutation in a sequence 3&#8242; to the coding region in which AATAAA is converted to AACAAA. Consequently, the amount of mRNA for &#946;-globin is decreased to 10% of normal. Which of the following functions in mRNA synthesis and processing is most likely encoded by the sequence AATAAA?

a) capping with GTP
b) cleavage and polyadenlyation
c) silencing the promoter
d) splicing of the initial mRNA transcript in the nucleus
e) transport of the mRNA out of the nucleus


 

VisionaryTics

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37.
A 5-year-old girl is brought to the physician because of listlessness, fatigue, and dull pain in the right upper quadrant of the abdomen. Her height and weight are below the 25th percentile. Laboratory findings indicate that the content of her &#946;-globin chain is 15% to 20% of normal. Sequencing of the &#946;-globin gene shows a point mutation in a sequence 3&#8242; to the coding region in which AATAAA is converted to AACAAA. Consequently, the amount of mRNA for &#946;-globin is decreased to 10% of normal. Which of the following functions in mRNA synthesis and processing is most likely encoded by the sequence AATAAA?

a) capping with GTP
b) cleavage and polyadenlyation
c) silencing the promoter
d) splicing of the initial mRNA transcript in the nucleus
e) transport of the mRNA out of the nucleus


B. It's the polyadenylation sequence. Pg. 75 in FA.
 
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need help in these

1 - 8 years old boy , 1 year of and self mutilation , his male cousin has the same , biting finger , spasticity ???


2- role of tretinoin in collagen synthesis ????
 

VisionaryTics

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need help in these

1 - 8 years old boy , 1 year of and self mutilation , his male cousin has the same , biting finger , spasticity ???


2- role of tretinoin in collagen synthesis ????
1-Lesch-Nyhan
2-Binds to nuclear receptors -> regulation of transcription
 
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missmedschool

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1. B (postcentral gyrus / somatosensory cortex)
2. depression
3. myasthesia gravis => deplete ACh as the day progresses => diaphragm becomes paralyzed => hypoventilation (hypoxemia, hypercapnia) and respiratory acidosis
4. HbF has increased affinity for O2 (which would be beneficial, because sickling is induced by hypoxia)
This tripped me up because I don't think I've ever been asked to identify the postcentral gyrus on the RIGHT side of the brain :confused: ugh I guess I'm just used to it being a nice pretty contiguous line like on the left side. That or the placement of "B" seemed to separate the upper half of the brain from the lower half so I assumed they couldn't really be connected. Sigh. :bang:
 

missmedschool

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If anyone can help me with the below questions I would be too happy. Thanks!

1. The peptidyl transferase question. Was the answer "attachment of amino acids to tRNA"? I got tripped up by the whole 60S 80S stuff

2. A 33 year old woman who is right-handed is brought to the physician because of a 3-day history of progressive weakness and numbness of her arms and legs. Neurologic examination shows proximal and distal weakness of the upper and lower extremities. There is areflexia. Sensation to vibration and joint position is decreased in the fingers and toes. Nerve conduction studies show a slow conduction velocity in the median, ulnar, peroneal, and tibial nerves. These electrophysiologic findings most likely indicate impaired function of which of the following ion channels?

a) neurotransmitter-gated Ca+2 channels
b) neurotransmitter-gated Na+ channels
c) neurotransmitter-gated K+ channels (WRONG )
d) Voltage-gated Ca+2 channels
e) Voltage-gated Na+ channels
f) Voltage-gated K+ channels

Could someone please explain the pathophys behind this?

3. A 46 year old man receives diagnosis of SCC of the esophagus. A barium swallow is shown Esophagectomy at the region (there was an accompanying image) is most likely to involve ligation of arterial branches of which of the following vessels?
a. aorta
b. internal thoracic artery
c. pulmonary arteries
d. SMA
e. thyrocervical trunk

4. In order to determine risk factors for death from coronary artery dz persons aged 30 yrs and older are studied in a community. Every 2 yrs for a total of 10 yrs BP, cholesterol, smoking status is assessed along with deaths from CAD Persons with increased BP are compared to those with normal BP to determine which group has greater mortality from CAD. Which of the following best explains this study?
a. case control
b. case series
c. cross sectional
d. ecologic
e. observational cohort
f. randomized clinical trial

Would appreciate if someone explained this one to me--> I was stuck between observational cohort and cross sectional

5. There was one about an Asian woman who took acetaminophen and alcohol together, she had acetiminophen toxicity and it wanted to know what was alcohol's effect. The answer choices were
a. decreased generation of nacetyl p benzoquinoeimine
b. increased glucoronidation
c. increased hepatic glutathione stores
d. increased sulfation
e. induction of cp450

6. One showed a tracing of a skeletal mm preparation and it asked which one had the highest amount of calicum sequestration?

7. A 60 year old woman with 2 day history of flank pain and pain with urination. She has HTN, recurrent UTIs, hypothyroidism ... normal temperature ... urinalysis 3+ blood, 1+ leukocytes, few bacteria. Imaging shows large calculus filling the entire right renal pelvis. What is the calculus most lkely composed of?

a. calcium oxalate
b. cystine
c. struvite
d. uric acid

I put calcium oxalate because she had no fever, so I thought struvite couldn't be right, but ... yeah. It was wrong. Explanation on this please?
 

VisionaryTics

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If anyone can help me with the below questions I would be too happy. Thanks!

1. The peptidyl transferase question. Was the answer "attachment of amino acids to tRNA"? I got tripped up by the whole 60S 80S stuff

Don't get confused. If you screw up protein synth, you make less protein. -edit- Confused this with a different question. Yeah, ijn is right. Peptidyltransferase is peptide bond formation between amino acids.

2. A 33 year old woman who is right-handed is brought to the physician because of a 3-day history of progressive weakness and numbness of her arms and legs. Neurologic examination shows proximal and distal weakness of the upper and lower extremities. There is areflexia. Sensation to vibration and joint position is decreased in the fingers and toes. Nerve conduction studies show a slow conduction velocity in the median, ulnar, peroneal, and tibial nerves. These electrophysiologic findings most likely indicate impaired function of which of the following ion channels?

a) neurotransmitter-gated Ca+2 channels
b) neurotransmitter-gated Na+ channels
c) neurotransmitter-gated K+ channels (WRONG )
d) Voltage-gated Ca+2 channels
e) Voltage-gated Na+ channels
f) Voltage-gated K+ channels

Could someone please explain the pathophys behind this?

Decreased nerve velocity means that regardless of what's going on at the dendrite/NMJ, conduction is screwed up. Saltatory conduction relies on voltage-gated Na+ channels at the Nodes of Ranvier.

3. A 46 year old man receives diagnosis of SCC of the esophagus. A barium swallow is shown Esophagectomy at the region (there was an accompanying image) is most likely to involve ligation of arterial branches of which of the following vessels?
a. aorta
b. internal thoracic artery
c. pulmonary arteries
d. SMA
e. thyrocervical trunk

Just straight anatomy. Esophageal arteries are branches of the aorta (with a little bit of supply inferiorly by the left gastric, which wasn't listed).

4. In order to determine risk factors for death from coronary artery dz persons aged 30 yrs and older are studied in a community. Every 2 yrs for a total of 10 yrs BP, cholesterol, smoking status is assessed along with deaths from CAD Persons with increased BP are compared to those with normal BP to determine which group has greater mortality from CAD. Which of the following best explains this study?
a. case control
b. case series
c. cross sectional
d. ecologic
e. observational cohort
f. randomized clinical trial

Would appreciate if someone explained this one to me--> I was stuck between observational cohort and cross sectional

Cohort. Cohorts take a population, and follow them forward in time (What will happen?). They are good for following up on sequelae of rare exposures. Cross-sectional studies have no time component; they are just surveys (What is happening?).

5. There was one about an Asian woman who took acetaminophen and alcohol together, she had acetiminophen toxicity and it wanted to know what was alcohol's effect. The answer choices were
a. decreased generation of nacetyl p benzoquinoeimine
b. increased glucoronidation
c. increased hepatic glutathione stores
d. increased sulfation
e. induction of cp450

Acetaminophen toxicity is mediated by a toxic metabolite that is produced after CYP450 metabolism of acetaminophen. Chronic alcohol use induces CYP450 -> increases conversion of acetaminophen to NAPQI (toxic metabolite).

6. One showed a tracing of a skeletal mm preparation and it asked which one had the highest amount of calicum sequestration?

It was the one were you could see the spaces between the contractions. The spaces meant that calcium was being sequestered into the sarcoplasmic reticulum between stimulations. When there were no gaps between contractions, the ability of the calcium sequestration pumps to remove Ca2+ from the cytoplasm was overwhelmed.

7. A 60 year old woman with 2 day history of flank pain and pain with urination. She has HTN, recurrent UTIs, hypothyroidism ... normal temperature ... urinalysis 3+ blood, 1+ leukocytes, few bacteria. Imaging shows large calculus filling the entire right renal pelvis. What is the calculus most lkely composed of?

a. calcium oxalate
b. cystine
c. struvite
d. uric acid

I put calcium oxalate because she had no fever, so I thought struvite couldn't be right, but ... yeah. It was wrong. Explanation on this please?

Staghorn calculi are almost always struvite stones caused by urease-producing bacteria.
herp
 
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ijn

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1. Aminoacyl-tRNA synthetase attaches amino acids to tRNA. Peptidyl transferase forms linkages between amino acids on the growing peptide chain.

2. Voltage gated sodium channels. It was honestly a guess when I originally took it. I know the answer is a voltage gated channel because condunction velocity is slower, but I'm not sure how they decided it couldn't be potassium. I guess if you had a potassium channel defect they'd be talking about how movement on repeated stimulation was imparied b/c of slow repolarization. Or maybe they'd be talking about some sort of long QT symptoms.

3. The aorta directly supplies blood to the esophagus.

4. Observational cohort

5. Chronic alcoholism induces cytochrome P450, therefore increasing the rate of glutathione depletion by acetaminophen => increased hepatotoxicity

6. Edit: oops, read it wrong. Definitely the one with the most peaks and valleys. A.

7. Struvite stones can get large enough to fill the whole renal pelvis. Calcium oxalate stones don't get that large and aren't associated with UTIs.

 

Drteeth21

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hey everyone! so my test is on wednesday and I'm totally freaking out. anyone hear anything about it this past month? I've taken pretty much all the nbmes at this point 13 last week and just took 12 and shooting for a 250. ive been in the 240s for 12 and 13.
anyone know anything?!
 

VisionaryTics

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hey everyone! so my test is on wednesday and I'm totally freaking out. anyone hear anything about it this past month? I've taken pretty much all the nbmes at this point 13 last week and just took 12 and shooting for a 250. ive been in the 240s for 12 and 13.
anyone know anything?!
I know lots of things.
 
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missmedschool

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OK so for the peptidyl transferase one the answer is "establishment of covalent bonding between amino acids" ... ?

& thanks VisionaryTics and ijn! :D
 
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The little girl with periorbital edema who was peeing protein after a URI for the past 2 weeks. No RBC or WBC in urine. They were selling PSGN hard and I know the answer was loss of neg charge of basement membrane.

My question: if PSGN makes you pee protein from the IC damage to the BM, why isnt it considered a nephrotic? (philosophic velociraptor pose)

Also dumb question: when they say "+10" what does this mean? Is it just an absolute number or does it have units? If so What units is it in?
 

frankyazz

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The little girl with periorbital edema who was peeing protein after a URI for the past 2 weeks. No RBC or WBC in urine. They were selling PSGN hard and I know the answer was loss of neg charge of basement membrane.

My question: if PSGN makes you pee protein from the IC damage to the BM, why isnt it considered a nephrotic? (philosophic velociraptor pose)

Also dumb question: when they say "+10" what does this mean? Is it just an absolute number or does it have units? If so What units is it in?
Because loss of negative charge isn't PSGN, its minimal change disease, which IS a nephrotic syndrome. Plus there were no RBC so you should know it wasn't a nephritic syndrome.
 

sunyD

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Sorry was looking at page 1...
 
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5.
A 77-year-old woman dies in the hospital after a long illness. Her vertebral column, obtained at autopsy, is shown in the photograph. The process shown is most likely associated with an increase in which of the following?

A) Calcium
B) Estrogen
C) Interleukin-1 (IL-1)
D) Monoclonal immunoglobulin
E) Vitamin D

??
 

frankyazz

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5.
A 77-year-old woman dies in the hospital after a long illness. Her vertebral column, obtained at autopsy, is shown in the photograph. The process shown is most likely associated with an increase in which of the following?

A) Calcium
B) Estrogen
C) Interleukin-1 (IL-1)
D) Monoclonal immunoglobulin
E) Vitamin D

??
Don't remember the picture exactly, but I think it was osteoporosis, so IL-1 which is a stimulator of osteoclasts. If it was a picture of multiple myeloma, then it would be D.
 

ruiner

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1. Aminoacyl-tRNA synthetase attaches amino acids to tRNA. Peptidyl transferase forms linkages between amino acids on the growing peptide chain.

2. Voltage gated sodium channels. It was honestly a guess when I originally took it. I know the answer is a voltage gated channel because condunction velocity is slower, but I'm not sure how they decided it couldn't be potassium. I guess if you had a potassium channel defect they'd be talking about how movement on repeated stimulation was imparied b/c of slow repolarization. Or maybe they'd be talking about some sort of long QT symptoms.

3. The aorta directly supplies blood to the esophagus.

4. Observational cohort

5. Chronic alcoholism induces cytochrome P450, therefore increasing the rate of glutathione depletion by acetaminophen => increased hepatotoxicity

6. Edit: oops, read it wrong. Definitely the one with the most peaks and valleys. A.

7. Struvite stones can get large enough to fill the whole renal pelvis. Calcium oxalate stones don't get that large and aren't associated with UTIs.

is that supposed to look like a dinosaur? cause it does


couple questions that haven't been asked:

lle thrombus removed, specimen shows scattered mesenchymal cells in abundant extracellular matrix. - cardiac tumor most likely:

A)fibroelastoma
B)fibroma
C) hamartoma
d) Hemangioma
e) Myxoma

only heart tumors i remember from FA/Uworld are myxoma and rhabodmyomas, didn't think it fit myxoma so guessed fibroma and am thinking it was probably fibroelastoma?

the one about the guy with paint thinner metabolic acidosis. i guess if i knew what paint thinner was i could probably answer this

this one is probably pretty dumb but i think i over thought it:
burning pain with urination, physical exam shows uterine prolapse, mild wbc in urine, bilateral dilation of renal collecting system. greatest risk for:

cervical carcinoma
pyelonephritis
renal cell carcinoma
ureterolithiasis
urothelial carcionoma

i put uretolithiasis because i was thinking well maybe this predisposes her to infection, rather then just putting pyelonephritis which i think is the answer

23 year old with yellow eyes, low grade fever, nasal congestion, muscle aches, everything else negative, high total, low direct bili, so high indirect bil

gilbert syndrome
hepatitis d
hereditary spheorcytosis
idiopathic cirrhosis
steatohepattis

i put hs but now that i look again i am thinking it was gilbert. obvious its an unconguatedbilirubenima
 

frankyazz

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is that supposed to look like a dinosaur? cause it does


couple questions that haven't been asked:

lle thrombus removed, specimen shows scattered mesenchymal cells in abundant extracellular matrix. - cardiac tumor most likely:

A)fibroelastoma
B)fibroma
C) hamartoma
d) Hemangioma
e) Myxoma

only heart tumors i remember from FA/Uworld are myxoma and rhabodmyomas, didn't think it fit myxoma so guessed fibroma and am thinking it was probably fibroelastoma?

the one about the guy with paint thinner metabolic acidosis. i guess if i knew what paint thinner was i could probably answer this

this one is probably pretty dumb but i think i over thought it:
burning pain with urination, physical exam shows uterine prolapse, mild wbc in urine, bilateral dilation of renal collecting system. greatest risk for:

cervical carcinoma
pyelonephritis
renal cell carcinoma
ureterolithiasis
urothelial carcionoma

i put uretolithiasis because i was thinking well maybe this predisposes her to infection, rather then just putting pyelonephritis which i think is the answer

23 year old with yellow eyes, low grade fever, nasal congestion, muscle aches, everything else negative, high total, low direct bili, so high indirect bil

gilbert syndrome
hepatitis d
hereditary spheorcytosis
idiopathic cirrhosis
steatohepattis

i put hs but now that i look again i am thinking it was gilbert. obvious its an unconguatedbilirubenima
myxomas are of mesenchymal origin. cervical carcinomas can invade bladder/ureter and cause bilateral dilation of renal collecting system (most common cause of death in cervical caner is post renal azotemia) . And yes probably gilberts. I took this a while ago so I don't exactly remember the questions with the descriptions you gave. Apologies if I am incorrect on anything.
 
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VisionaryTics

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myxomas are of mesenchymal origin. cervical carcinomas can invade bladder/ureter and cause bilateral dilation of renal collecting system (most common cause of death in cervical caner is post renal azotemia) . And yes probably gilberts. I took this a while ago so I don't exactly remember the questions with the descriptions you gave. Apologies if I am incorrect on anything.
It was pyelonephritis from urinary stasis. Yes, cervical CA can cause urinary status, but urinary stasis isn't a risk factor for it.
 

ruiner

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thanks guys. im pretty much my worst enemy on this thing so far. all 3 i should have had. do now now hopefully not on the test.
 

takethat12

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Don't remember the picture exactly, but I think it was osteoporosis, so IL-1 which is a stimulator of osteoclasts. If it was a picture of multiple myeloma, then it would be D.
Wait was it osteoporosis or was it too much bone deposition? I couldn't tell. The vertebrae looked osteopenic but then it looked like there was bridging bone around the discs.

Anyone remember the correct answer to this question?
 

Zarika

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This is kind of a dumb one, but I'm not sure on the answer...

Woman presents to ED with difficulty breathing and severe muscle wekaness for 10 minutes. She has three year history of MG treated with neostigmine. Husband reports se doubled her dosage 2 days ago b/c she was feeling extraordinary weak, but her weakness has increase since then. Which of the following events is the most likely cause of the increased muscle weakness in this patient?
A) Autoimmune hyperactivation of nicotinic rec
B) AI inactivation of muscarinic receptors
C) desensitization of nicotinc receptors
D) excessive degradation of ACh
E) hypersensitization of muscarinic receptors
F) insufficient release of acetylcholine
 

ipizzy

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C - she doubled her neostigmine dose and is now desensitized to acetylcholine
 

Zarika

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Thanks, I put E thinking it was some kind of feedback thing
 

Radonkulous

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I have a few questions that I haven't come across in the thread. Thanks in advance:

2.8: One regarding woman with enlarged uterus. What is next stop of establishing diagnosis
measure fsh, tsh, hcg, ultrasound, biopsy. I put ultrasound. Thought it was mole.

2.18: Man with cirrhosis who has erectile dysfunction. What is decreased?
estradiol, estrone, fsh, hcg, lh, testosterone. I thought it was lh but my guess it is testosterone.

2.39: man presents to ed with bruit in lower abdomen. what is going on?
compression fracture, herniated disc, leaking aortic aneurysm, leaking renal artery aneursym, perforated rectum, perforated sigmoid colon. Thought it was renal artery aneurysm

3.16: 2 month old dies of meningitis (mycobacterial infection). What is going on?
Brutons agammaglobulinemia, leukocyte adhesion deficiency, complement deficiency, ifn-gamma receptor problem. I put leukocyte adhesion deficiency.

3.35: male newborn overreacts to stimuli and has startle response. What was mother using?
heroin, lsd, marijuana, alcohol, psilocybin. Put marijuana

4. 19: traveler has watery diarrhea. What do you do to find what he has?
culture the stool, EM of stool for viruses, microscopic examination of stool for ova and parasites, PCR for shiga toxin, rectal biopsy

4.21: man doesnt want diabets. what should be his diet?
low calorie, low carb, low protein, low cholesterol, low protein, low sodium

4. 29: locate portion of brain which is responsible for decreased touch sensation. not much help without picture

4.47: mouse has fasting hypoglycemia not corrected with glucagon but with epinephrine. Whats defective?
adenylyl cyclase, glucagon receptor, glycogen phosphorylase, heterotrimeric G protein, phosphorylase kinase, protein kinase a

Thanks again in advance!!!!!
 

Dr McSexy

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I have a few questions that I haven't come across in the thread. Thanks in advance:

2.8: One regarding woman with enlarged uterus. What is next stop of establishing diagnosis
measure fsh, tsh, hcg, ultrasound, biopsy. I put ultrasound. Thought it was mole.

If that's the one where it says something about a blue tinged vaginal mucosa, then hCG is the right answer. I guessed at that one, but I had defaulted to the always check to see if pregnant rule.

2.18: Man with cirrhosis who has erectile dysfunction. What is decreased?
estradiol, estrone, fsh, hcg, lh, testosterone. I thought it was lh but my guess it is testosterone.
yes it's testosterone. Alcohol causes increased aromatization of testosterone to estrogen, leading to gynecomastia, spider anigomas, etc. Decreased testosterone as a result and its assoc. effects.

2.39: man presents to ed with bruit in lower abdomen. what is going on?
compression fracture, herniated disc, leaking aortic aneurysm, leaking renal artery aneursym, perforated rectum, perforated sigmoid colon. Thought it was renal artery aneurysm
leaking aortic aneurysm

3.16: 2 month old dies of meningitis (mycobacterial infection). What is going on?
Brutons agammaglobulinemia, leukocyte adhesion deficiency, complement deficiency, ifn-gamma receptor problem. I put leukocyte adhesion deficiency.
ifn-gamma receptor problem. ifn-gamma is needed to fight mycobacteria.

3.35: male newborn overreacts to stimuli and has startle response. What was mother using?
heroin, lsd, marijuana, alcohol, psilocybin. Put marijuana
answered on the previous page. Heroin

4. 19: traveler has watery diarrhea. What do you do to find what he has?
culture the stool, EM of stool for viruses, microscopic examination of stool for ova and parasites, PCR for shiga toxin, rectal biopsy
It mentioned hiking which is a buzz word for giardia. So check stool for ova and parasites

4.21: man doesnt want diabets. what should be his diet?
low calorie, low carb, low protein, low cholesterol, low protein, low sodium
answered previously, low calorie

4. 29: locate portion of brain which is responsible for decreased touch sensation. not much help without picture
B is the answer. Answered previously and there's a picture in this thread I'm pretty sure

4.47: mouse has fasting hypoglycemia not corrected with glucagon but with epinephrine. Whats defective?
adenylyl cyclase, glucagon receptor, glycogen phosphorylase, heterotrimeric G protein, phosphorylase kinase, protein kinase a
answered previously. glucagon receptor

Thanks again in advance!!!!!
..
Those should be it, unless I'm mis-remembering my answers or questions.
 
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