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Welcome to meningitisโ€™s page.
Contributor score: 644


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 +1  visit this page (nbme23#16)
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The question is confusing because a TRUE POSITIVE test result is finding detecting cancer by US (goes to show you we gotta look at what the test is looking for).

An ABNORMAL test detecting PrCa means its NOT A POSITIVE: ie: 35 out of 50 were False Positives

An ABNORMAL test WITHOUT PrCa means its NOT A NEGATIVE: 20 out of 100 WITHOUT PrCa were FALSE NEGATIVE.

TN = 80, FP = 15. Specificity: TN/(TN+FP); 80/(80+15) = 84%. And since it says "best represents" then 84% is closest to 80%.

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 +3  visit this page (nbme22#11)
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Actually, I correct myself: I looked closer and the Genito femoral has an external Spermatic branch and a Lumboinguinal branch. I thought it was the Genitofemoral nerve because the genital branch passes through the deep inguinal ring, enters the inguinal canal, goes to spermatic cord and supplies the cremaster and scrotal skin.

Heres the image: https://upload.wikimedia.org/wikipedia/commons/e/e4/Gray824.png

Correct me if I am wrong please.

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gh889  I think you're right, FA2019 pp444 even states that sensory to the scrotum is via the Genitofemoral nerve +5

 -4  visit this page (nbme22#30)
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Process of elimination on this one.

  • I eliminated Carbomyl phosphate, Arginine due to urea cycle.
  • I eliminated ATP because ATP alone wouldn't change F6P into glucosamine
  • NAG I got lucky and I eliminated it due to its use in ECM and collagen so I didn't think it was relevant and I kind of remembered it being in urea cycle.
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dr.xx  you mean, pure luck? :) +13
impostersyndromel1000  lol pretty sound logic here mate +3
nor16  same here, Glutamine is a NH3 (-amin) donor, so guessing made sense +

 +4  visit this page (nbme22#38)
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Although itโ€™s about PPV, this researching helped me understand basic phys, I hope this helps everyone in some way.

Takeaway: During PPV, venous return decreases, cardiac output decreases, and heart pressures decrease in the right side of the heart.

Why does PPV decrease venous return?

  • intrathoracic pressure compresses heart, causing blood not to return

Causes for decreased left ventricular output during ventilation:

  • Shifting of intraventricular septum to Left due to increased RV volume
  • Decreased venous return
  • Changes in hearts ability to contract due to positive pressure
  • lack of O2 to heart

Normal compensatory mechanisms for maintaining CO and BP during PPV?

  • increased HR to compensate for decreased SV
  • increased SVR to maintain BP

Other Physiologic responses:

  • Decreased cerebral perfusion pressure (bodyโ€™s response to a fall in CPP is to raise systemic blood pressure and dilate cerebral blood vessels)
  • Decreased renal perfusion (Increased ADH, RAAS, and Patient has renal problems so increased creatinine and uric acid)
  • Possible malnutrition (increased glucose via gluconeogenesis etc.)
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meningitis  sorry about the formatting, they were supposed to be bullets not italic. +30
drdoom  looks good to me! ;) instead of asterisks try using the plus sign for unordered lists; the system gets confused sometimes because the asterisk is also for italics ๐Ÿ˜Š +2
meningitis  Yeah, I noticed :s Oh, I didnt know the + sign did that! Very much appreciated, I will try that next time. +1

 +6  visit this page (nbme22#32)
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A case control study cant assess the prevalence of a disease but a cross sectional study can.

  • A case control study is that you are setting the margins in the 2 by 2 table therefore you're deciding how many cases and controls you want to have in your study and the calculation of incidence / prevalence in this scenario would be biased.
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meningitis  the prevalence of the exposure and the health outcome are measured at the same time. You are basically trying to figure out how many people in the population have the disease and how many people have the exposure at one point in time. Case Control would determine ODDS ratio Cohort would determine Relative Risk +3

 +4  visit this page (nbme22#30)
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I thought: lower pole then cant be suprarenal nor stomach which are higher""

Duodenum and Body of pancreas (except tail) are retroperitoneal and midline

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makinallkindzofgainz  I ruled out duodenum because it's towards the right side, and I ruled out body of pancreas because that's basically midline. We are talking about the left lower kidney, which is by the spleen and splenic flexure. Idk if this logic checks out, but I got it right +
chaosawaits  The only part that frustrated me about this picture is that the stomach is incredibly variable in its final resting place within the population and, as the picture provided on this page shows, the splenic flexure is a bit lateral to the kidneys. So I overthought it and chose not-so-wisely +

 +6  visit this page (nbme22#19)
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Ewing sarcoma cells look like small blue hypercromatic cells because they are neuroectodermal origin (PNET) and are therefore undifferentiated with high N:C ratio.

Also remember 22+11 translocation (EWS gene on chromosome 22 and the FLI-1 gene on chromosome 11)

Yeah, I thought the same @praderwilli (about the concentric layers)

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kevin  just for people who are taking exam this year, ewing is now understood to be mesenchymal stem cell neoplasm (uworld) +3

 +3  visit this page (nbme22#11)
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"Pick your Big, Foamie, Zeibra nose with your Sphinger"

Choose options with the letter I.

SpIngomyelin, Sphingomyelinase, bIgorgans (hepatomegaly etc), zeIbra bodies, Foam cells

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 +18  visit this page (nbme22#18)
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Tanner stages start at TEN years old

Stage I:

  • I is flat, as in flat chest;
  • I is alone, as in no sexual hairs.

Stage II (2): stage II starts at 11 y/o (II look like 11)

  • 2 balls (testicular enlargement)
  • 2 hairs (pubic hairs now appearing)
  • 2 breast buds form

Stage III (3): starts at 13 y/o

  • If you rotate 3, it looks like small breasts (Breast mounds form);
  • If you squiggle the III they look like curly+coarse pubic hair
  • Increased penis length and size can be represented by: II --> III
    (your penis was thin II but now its thicker III)

Stage IV (4): starts at 14 y/o

  • First imagine: The I in IV represents the thigh, and the V in IV looks like the mons pubis between your legs:
    MEANING: you have hair in mons pubis (V) but you have a border detaining the hair from growing into thighs.
  • The V is pointy, as in now the breasts are pointy (raised areola or mound on mound)

Stage V (5): 15 y/o

  • V has no borders detaining hair from growing into thighs (pubic hair + thigh hair)
  • 5 fingers(as in hands) flattening the areolas when grabbing them (areola flatten at this stage and no more "mound on mound")

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meningitis  Sorry about the format, it came out wrong but I hope his helps. +2
drdoom  looks good to me! +25
gh889  According to FA2019, stage 2 ends at 11, stage 3 starts 11.5-13, and stage 4 starts at 13-15, where did you get your info from? +1
meningitis  You can change it to ENDS at 11, ENDS at 13, ENDS at 14... I simply have it as a range just like you stated in a couple of them. The importance is in how the kid presents because he/she will have some things mature but others not, the age will vary in questions. +1
endochondral1  stage 3 breast mound is for females not males btw +4
endochondral1  see pg. 635 in FA it just pubertal. Idk if that correlates to the same stage as females +1
angelaq11  this is just too funny, I LOVE it! xD +4
snripper  While this is impressive, this doesn't help with answering the question. +2
yng  Pseudogynecomastia (False gynecomastia): this has nothing to do with puberty or hormones. Simple d/t the fast some guys have extra fat in chest area, making it look like they have breasts. The boy weight at 60 percentile while height at 50 percentile. +1

 +0  visit this page (nbme22#20)
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I think the small dark area on the left head of femur and the darkened neck are the avascular sites.

Neck: http://img.medscapestatic.com/pi/meds/ckb/15/19515tn.jpg

Head: (obvious lesion on the RT femur, but similar discrete lesion on the left as seen on the practice NBME) http://radsource.us/wp-content/uploads/2005/11/1a.jpg

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 +9  visit this page (nbme22#26)
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hydrocholorothiazide is DOC for Nephrogenic Diabetes insipidus because it paradoxically causes an increase in BP by increasing sodium absorption and thus water absorption, Pathoma explains this nicely.

Desmopressin is incorrect because upon fasting (fluid restriction) ADH is increased meaning ADH is being released Centrally but is not working in the kidneys at the V2 receptors of the epithelial renal cells at Collecting duct.

On that note, Amiloride is used for Lithium induced nephrogenic DI.

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hello  Where in Pathoma? I couldn't find it. +2
almondbreeze  also sketchy says that thiazide s decrease the amount of lithium cleared--> lithium toxicity +2
paperbackwriter  Agh confused as well because FA2019 (pg 562) says that thiazides are implicated in lithium toxicity D: +1
paperbackwriter  OOPS, please ignore last comment. I just realized that this Q stem never mentioned lithium. And on top of that @meningitis mentioned that amiloride is used if lithium induced. Apologies. +1
jaramaiha  Question is nephrogenic DI. ADH is increased but kidney's aren't reacting, mutated receptors. In which the Tx is HCTZ +1

 +12  visit this page (nbme22#1)
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I also thought the same as @bubbles, but now trying to "justify" this tricky NBME question: I think this revolves on the fact that the patient has a HIGH blood pressure meaning we should focus on an answer that explains both increased BP and Hypovolemia (i.e: increased ADH which vasoconstricts and also absorbs free-water, both of which increase BP and cause hypovolemia).

Maybe if this patient were decompensated with LOW BP, one could think more about ANP.

I still think this question is TOO tricky.

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meningitis  Sorry, hyponatremia* right? +1
mantarayray  I think that it's not ANP because ANP will cause a loss of Na but water will follow (they usually go together), whereas ADH will cause absorption of only water and will cause hyponatremia except only thought this post getting the question wrong :") +5
mantarayray  Oops sorry the formatting is confusing: I think that it's not ANP because ANP will cause a loss of Na but water will follow (they usually go together), whereas ADH will cause absorption of only water and will cause hyponatremia. +4
pg32  @mantaray pretty sure you are right and that is the only way to get this question correct. Remembering that Na concentration really is a measure of water balance is key. If the pt is hyponatremic, that just means they have too much water in the blood, which is caused by ADH. If the patient was hypoVOLEMIC, that might mean they are losing too much Na. This is illustrated by pts with SIADH. They are hyponatremic, but euvolemic, meaning that they have too much water (hyponatremia from the ADH) but their Na balance is ok (due to excretion of Na via ANP/BNP) +1
avocadotoast  We need to be thinking about how heart failure is a condition with a low effective circulating volume. Our patient had an MI and now his heart cant keep up with the volume (low CO), leading to congestion. When congestion occurs, water is pushed into the interstitial spaces and isn't circulating in the arterial system. For that reason, the body ramps up the RAAS and ADH despite an actual increase in body water. This is a non-osmotic release of ADH. At this point plasma sodium levels are determined by relative intake and losses and hyponatremia is common in these patients because of that. Also, ANP and BNP don't hold a candle to the RAAS. +1

 -8  visit this page (nbme21#23)
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Squamous and Small cell carcinomas are Sentral (central) and often caused by Smoking

Hilar mass C arising from bronchus; Cavitation; Cigarettes; hyperCalcemia (produces PTHrP). Keratin pearls D and intercellular bridges.

pg 669 2019 FA

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 +10  visit this page (nbme21#46)
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LPS found in outer membrane of gram โŠ bacteria (both cocci and rods). Composed of O antigen + core polysaccharide + lipid A (the toxic component).

Activates Macrophages and induces TNFalpha release -> Hypotension and fever.

Pg 133 Endotoxin.

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zevvyt  and just to note answer b) "induction of histamine release" DOES happen , but it's not the "Initial Event" that the question asks for +1
unknown001  there you go, another introducer of confusion who dislikes straightforward questions +

 +22  visit this page (nbme20#50)
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When standing up, the body normally activates sympathetic system to avoid orthostatic hypotension.

But since there is now an additive effect of the pheochromocytoma adrenergics, it will lead to a hypertension

(i.e: Double vasoconstriction = Pheo adrenergics + Sympathetic system)

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sympathetikey  Brilliant. +6
medschul  Would pheo have a normal resting BP though? +16
meningitis  I was trying to justify these tricky questions but very true medschul.. It shouldn't have normal resting BP. Sometimes it seems these NBME always have a trick up their sleeve. Im getting paranoid lol +
nala_ula  The reason why the patient probably has normal HTN is because Pheochromocytoma has symptoms that occurs in "spells" - they come and go. Apparently in that moment, when the physician is examining her, she doesn't have the HTN, but like @meningitis explained, so many adrenergic hormones around leads to double the vasoconstriction when the patient stands up. +10
meningitis  Thank you @nala_ula for your contribution! Really filled in the gap Iwas missing. +2
nala_ula  No problem! Thank you for all your contributions throughout this page! +2
mjmejora  I thought the pheochromocytoma was getting squeezed during sitting and releasing the epinephrine then. kinda like how it can happen during manipulation during surgery. Got it right for sorta wrong reasons then oh well. +
llamastep1  When she sits in the examination table there would be a normal activation of the sympathetic system from the stress of getting examined which is amplified by the pheo. Cheers. +
sammyj98  UpToDate: Approximately one-half have paroxysmal hypertension; most of the rest have either primary hypertension (formerly called "essential" hypertension) or normal blood pressure. +
hello_planet  FA 2019 pg. 336 +2
notyasupreme  Damn llama, that is WAYYY too much of an inference. Maybe if they said she was nervous in general or something, but not everyone gets stressed out by a doctor hahaha +
jakelong377  Itโ€™s not about being stressed infront of doctor. When u stand sympathetics activate to prevent orthostatic hypotension, to counter it adrenal medulla released catecholamines so much so that pheochromocytoma patients would appears with flushed skin n such +




Subcomments ...

submitted by step_prep5(246), visit this page
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  • Heat stroke: Elevated temperature with CNS dysfunction, caused by impaired thermoregulation
  • Heat exhaustion: Elevated temperature with no CNS dysfunction, caused by inadequate salt and water replacement
  • Malignant hyperthermia โ€“> Often seen in patient receiving anesthetic who develops hyperthermia and rigidity

https://step-prep.org/tutoring/

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etherbunny  When you say MH is "often seen" in patients receiving anesthesia, its VERY rare. +
meningitis  Im thinking he meant "often seen" in question stems.. not the actual incidence +


submitted by yotsubato(1208), visit this page
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Although acetaminophen (Tylenol) is not considered an NSAID, it too may provoke an aspirin-like sensitivity.

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meningitis  For that same reason (not an NSAID) it doesn't reduce inflammation so it cant be used for Gout. +7
meningitis  And I think Indomethacin is associated with anaphylactic reactions in patients with aspirin-sensitive asthma and aspirin allergies. Can anyone confirm? +1
link981  How many other's like me didn't see "allergic to aspirin"? FML +3
hyperfukus  OMFG me too i just got so mad and questioned my whole life at least its cuz i can't read not bc i don't understand :((((( +1
an1  Actually, from what I recall from UW, acetaminophen actually is an NSAID... it only acts centrally though. From FA: "Reversibly inhibits cyclooxygenase, mostly in CNS. Inactivated peripherally." But for that reason, It wouldn't be helpful for gout because it can't do squat in the periphery, which is where gout accumulates. +
freemanpeng  link981 Are u blind? +


submitted by mousie(272), visit this page
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A hemangioma is a type of benign (non-cancerous) tumor in infants. This abnormal cluster of small blood vessels appears on or under the skin, typically within one to three weeks after birth. - www.childrenshospital.org Hemangioma is a BV/capillary birthmark

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sympathetikey  Probably a Strawberry Hemangioma since she's a baby +10
meningitis  Can anyone explain what is option A? +2
redvelvet  bc, it's a benign "capillary" hemangioma, we can see "thin-walled blood vessels with narrow lumens filled with blood and separated by connective tissue". It sounds similar to "arterioles in a fibrous stroma" but it's capillary. +1
peridot  @meningitis I believe option A ("arterioles in a fibrous stroma") is describing an angiofibroma. The name angiofibroma already tells you that there is some component of fibrotic tissue involved, whereas in this case of strawberry hemangioma, the name tells you that it's more like pure blood vessels (capillaries in this case). +5
madamestep  @periodt Also those are pretty much always going to be in teen boys with recurrent nosebleeds! +


submitted by joonam(31), visit this page
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Acute or chronic inflammation of gallbladder. Murphy sign: inspiratory arrest on RUQ palpation due to pain. Pain may radiate to right shoulder (due to irritation of phrenic nerve).๔ฐALP if bile duct becomes involved (eg, ascending cholangitis).

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meningitis  To make sure, palpable Gallbladder is more in cholangiocarcinoma and Pancreatic Cancer? And if it were non-tender, could palpable gallbladder mean gallstones? +9
yb_26  @meningitis, it is a Courvoisier sign of pancreatic adenocarcinoma: jaundice + palpable, nontender gallbladder +3
an1  what's the periumbilical ecchymosis? could this be caput medusa? +
an1  and what about tenderness of the epigastrium on palpation? +
fatboyslim  @an1 Periumbilical ecchymosis is likely referring to Cullen's sign which is commonly associated with hemorrhagic pancreatitis. Another sign associated with hemorrhagic pancreatitis is Grey Turner sign, which is ecchymosis around the flanks bilaterally. +


submitted by sympathetikey(1600), visit this page
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Per FA (pg. 636): Concerning breast cancer...

"Amplification/overexpression of estrogen/ progesterone receptors or c-erbB2 (HER2, an EGF receptor) is common; ER โŠ, PR โŠ, and HER2/neu โŠ form more aggressive."

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sympathetikey  FA 2019 +5
meningitis  Why others not it: Anticipation: Trinucleotide repeats; CAG (Huntington), CTG (Myotonic dyst), GAA (ataxia telangiectasia), CGG(Fragile X) Chromosomal rearrangement: Many but can think of Trisomy 21, BCR-Abl, etc Imprinting: Prader willi, angelman Loss of heterozygosity: loss of a single parent's contribution to part of its genome. A common occurrence in cancer, it often indicates the presence of tumor suppressor gene in the lost region. +3
kai  trinucleotide repeats are not associated with breast cancer Neither are chromosomal rearrangements BRCA1,2 tumor supressor genes are associated with breast cancer, which is why I chose E, but I guess I should have bought the new First Aid.......... +
charcot_bouchard  GAA is Freidrich Ataxia +5
tulsigabbard  So is the amplification of the receptors unrelated to BRCA 1, 2? I'm still stuck on this as Sketchy states that breast cancer falls under the "two-hit" model. +
tallerthanmymom  @tulsigabbard I think one of the keys here is the question stem; " what is the most likely cause of the OVERexpression in this pts tumor cells?" --> I think that the "2-Hit" model would lead to UNDERexpression of a tumor suppression gene rather than overexpression. Whereas amplification would cause OVERexpression of the HER2/estrogen and progesterone receptors. But, I don't think that amplification would be the answer if they were asking about a triple negative cancer. +1
tallerthanmymom  Also this is on page 632 of FA 2018 for those using that version +
tulsigabbard  @tallerthanmymom - thank you! +
drzed  I can understand why @tulsigabbard dropped out of the race--she's taking step 1 soon LOL +3


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What are we supposed to be looking at? I see multinucleated giant cells. I also see infiltrate (canโ€™t tell if this is mononuclear or not).

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methylased  Young child following URI with TCP is pretty classic ITP. Sometimes they throw in extra stuff on purpose, but I didnโ€™t see much on the bone marrow aspirate either. +9
mousie  I was also thinking ITP but the bone marrow image kind of threw me off too, not sure what I'm supposed to see but still think ITP is best choice ... +
meningitis  It also almost threw me off, but then I remembered he had low platelet count and I guessed those multinucleated cells were Megakaryocytes (I looked for Megakaryocyte Bone Marrow Biopsy in google and they are the same). +1
what  Bone marrow shows increased megakaryocytes -> ITP +


submitted by thomasalterman(181), visit this page
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Androgens cause acne. Testosterone is a better answer than Androstanediol b/c the Testosterone is associated with puberty, Androstanediol is more associated with the adrenal glands.

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meningitis  I chose Testosterone but I almost chose GnRH because it is surged when starting puberty and therefore increases everything downstream. +11
temmy  When answering the question, i thought to myself that if GnRH is correct, LH will be too cos GnRH stimulates the Leydig cells via LH to release testosterone. That left testosterone as the best answer because it had the most direct effect. +11
goaiable  GnRH and LH are increased in a pulsatile fashion at the onset of puberty, so idk if that constitutes as the "rapid increase" that this question is asking for. Tripped me up also. +
tallerthanmymom  I originally eliminated testosterone and chose androstanediol because women can have Acne Vulgaris too, and Testosterone should not be rising to the same degree. Do I not understand how puberty works? +2
drzed  Women can still make testosterone though; and androstAnediOL is not the same as androstEnediONE +3


submitted by sympathetikey(1600), visit this page
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I see what they're saying (this was my second choice) but at the same time I feel like a backup of blood would activate the baroreceptors and cause decreased sympathetic activity to the SA & AV node.

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sympathetikey  (choice E) +
meningitis  Could you elaborate? Is this related to: less "preload" from mother circulation causes lowered HR? +
meningitis  Or backflow of blood and causes a Reflex Bradycardia? still confused on this question. +
kentuckyfan  So I think the subtle difference in choice E is that there would be a negative CHRONOTROPIC effect, no inotropic effect (contractility). +10
maxillarythirdmolar  if anything, inotrophy could go UP not down as diastole prolongs and LVEDV increases --> Starling equation bullshit +


submitted by thomasalterman(181), visit this page
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She just completed the course of rituximab, which targets CD20 receptors. B-cell deficiency can predispose to bacterial infections.

b) BM failure is not associated with rituximab c) wrong d) wrong e) this occurs w/in 7-10 days of starting treatment, and would not occur after completing a 4-month course of rituximab.

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meningitis  Forgot the time frame for Serum sickness and got it wrong.. thanks @thomasalterman +25
stinkysulfaeggs  Same. Crap. +2
medstudent22  Taking it one step further - B-cell depletion = decreased Ab secretion = decreased opsonization. Opsonization with subsequent phagocytosis by spleen = #1 mechanism by which encapsulated bacteria (ie Strep Pneumo) are degraded. +3


submitted by aesalmon(95), visit this page
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Leydig cell hyperplasia, should also see fibrosis and hylinazation of the tubules but i'm not seeing it... ยฏ_(ใƒ„)_/ยฏ

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meningitis  I think its there.. I thought it was the lighter red/pink material (hyaline material) And I thought the white streaks were the fibrosis like "streaked ovaries"in Turners. +
samadmom  Apparently the histology looks like leydig cell hyperplasia but is actually called "pseudoademonatous clusters" and are reduced in number due to increased FSH and LH. +


submitted by meningitis(644), visit this page
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Although itโ€™s about PPV, this researching helped me understand basic phys, I hope this helps everyone in some way.

Takeaway: During PPV, venous return decreases, cardiac output decreases, and heart pressures decrease in the right side of the heart.

Why does PPV decrease venous return?

  • intrathoracic pressure compresses heart, causing blood not to return

Causes for decreased left ventricular output during ventilation:

  • Shifting of intraventricular septum to Left due to increased RV volume
  • Decreased venous return
  • Changes in hearts ability to contract due to positive pressure
  • lack of O2 to heart

Normal compensatory mechanisms for maintaining CO and BP during PPV?

  • increased HR to compensate for decreased SV
  • increased SVR to maintain BP

Other Physiologic responses:

  • Decreased cerebral perfusion pressure (bodyโ€™s response to a fall in CPP is to raise systemic blood pressure and dilate cerebral blood vessels)
  • Decreased renal perfusion (Increased ADH, RAAS, and Patient has renal problems so increased creatinine and uric acid)
  • Possible malnutrition (increased glucose via gluconeogenesis etc.)
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meningitis  sorry about the formatting, they were supposed to be bullets not italic. +30
drdoom  looks good to me! ;) instead of asterisks try using the plus sign for unordered lists; the system gets confused sometimes because the asterisk is also for italics ๐Ÿ˜Š +2
meningitis  Yeah, I noticed :s Oh, I didnt know the + sign did that! Very much appreciated, I will try that next time. +1


submitted by mattnatomy(46), visit this page
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Severe hypertension often leads to hyperplastic arteriolosclerosis (onion-skin appearance). Also see proliferation of smooth muscle cells.

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meningitis  and explains the flame hemorrhages (Goljan) caused by malignant HTN +5
taediggity  FA 2020 pg. 537 +
dentist  FA 2020 pg 301* +
ally123  The flame hemmorhages are also a good buzz word for recognizing he has hypertensive retinopathy 2e chronic, uncontrolled HTN. Pt's with hypertensive retinopathy can also present with "cotton wool spots" and "macular star". Pics on FA 2019, p. 299 +2
surfacegomd  Pathoma (2018) p. 69 +
madamestep  @ally123 I think the best buzzword for hypertensive retinopathy here is "190/135 mmHg" +


submitted by k_tron_3000(35), visit this page
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Just a random factoid (as far as I know), in patients with pancreatitis the most likely vessel for thrombosis is the splenic vein due to close โ€œanatomic tiesโ€ with the pancreas. This would also cause gastro-splenic varices, explaining the vomiting of blood.

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meningitis  Also explains the splenomegaly. If you have thrombosed splenic vein, the blood will pool in the spleen, can also cause expansion of red pulp of spleen. +11
pg32  I picked splenic vein because of this ^^ association. However, why is the patient vomiting blood if there isn't a backup of blood into the left gastric/esophageal veinous system? +1
savethewhales  The splenic vein drains the fundus of the stomach. So, splenic vein thrombosis can cause gastric fundal varices, which explains his bloody vomit. +4
medschooler1  how do you rule out arteries? +
ac3  @medschooler1 Just my guess, but when answering this I assumed that splenomegaly meant splenic congestion with blood which can only happen if its outflow tract (splenic vein) is blocked. +5
thrawn  Arterial occlusion would be mesenteric angina - or the likes thereof. Venous occlusion leads to variceal bleed +
imgdoc  You rule out arteries because if they are occluded its an infarction and if they are partially occluded you'll get angina. +


submitted by atstillisafraud(217), visit this page
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Niemann-Pick Disease presents with mental retardation, lipid laden (foam cells) in bone marrow and cherry red spot on macula. No sphingomyelinase results in buildup of sphingomyelin which builds up in macrophages.

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meningitis  "Pick your **Big** **Foamie** **Zeibra** nose with your Sphinger" Choose options with the letter I. SpIngomyelin, Sphingomyelinase, bIgorgans (hepatomegaly etc), zeIbra bodies, Foam cells +2


submitted by moloko270(77), visit this page
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Myofibrils are composed of smaller structures called myofilaments. There are two main types of filaments: thick filaments and thin filaments; each has different compositions and locations. Thick filaments occur only in the A band of a myofibril. Thin filaments attach to a protein in the Z disc called alpha-actinin and occur across the entire length of the I band and partway into the A band.

https://opentextbc.ca/biology/chapter/19-4-muscle-contraction-and-locomotion/

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meningitis  isn't letter C the intercalated disc where the gap junctions are? +13
chediakhigashi  The actin is bound to structural proteins at the Z-line, this was on u-world #1734 if i understood correctly +


submitted by tissue creep(133), visit this page
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Arthropod for sure, but for the record I'm pretty sure this was Chikungunya Virus. Only got this from a UWorld question as I hadn't seen it until then, but apparently the arthralgia is really bad, which is what drew me to the answer.

https://www.cdc.gov/chikungunya/index.html

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meningitis  More like Zika Virus (Same a. aegypti vector) since it says she has rash associated to her bone and muscle pain. I had Zika one time (i live in Puerto Rico). Remember also dengue and Zika are Flavivirus. Dengue can cause hemolysis (hemorrhagic), and Zika is associated with Guillen Barre and fetal abnormalities. +12
nala_ula  I'm shocked that I found a fellow puerto rican on this site! Good luck on your test! +2
namira  dont be shocked! me too! exito! +2
niboonsh  Dengue is also known as "bone break fever" which makes me think its more likely to be dengue due to the "excruciating pains in joints and muscles". https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4242787/ +25
dr_jan_itor  I was thinking that its Murine typhus transmitted by fleas +
monique  I would say this is more likely scenario of either Dengue or Chikungunya, not Zika virus. Excruciating pain is common in those, not in Zika. Zika has milder symptoms of those three infection. +2
jakeperalta  Can confirm that Chikungunya's arthralgia is pretty horrible, from personal experience. +
almondbreeze  UW: co-infection with chikungunya virus with dengue virus can occure bc Aedes mosquito is a vector of both Chiungunya, dengue, and zika +
lovebug  FA2019, page 167 RNA virusesy. +
lovebug  Found that Chikungunya also have Rash./// An erythematous macular or maculopapular rash usually appears in the first 2โ€“3 days of the illness and subsides within 7โ€“10 days. It can be patchy or diffuse on the face, trunk and limbs. It is typically asymptomatic but may be pruritic (Taubitz W, Cramer JP, Kapaun A, et al. Chikungunya fever in travelers: clinical presentation and course. Clin Infect Dis. 2007; 45: e1. ) +1
beto  it is chikungunya->fever, polyarthralgia, diffuse macular rash, dengue has retro-orbital pain mostly +1


submitted by nosancuck(102), visit this page
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Dam son this lil b got some UMBILICATED Molluscum all up in her bizness

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drdoom  tru. +
meningitis  Pg 164 FA 2019 +1
dr.xx  likely not "lil b" as 2-4 times as many cases are found in whites than in persons of other races +7
drdoom  lil b not a referent of race; cf. lil boo, lil baybay, lil bowow, &c. +
dr.xx  I disagree. Google "lil b" for images. See what you may discover. +1


submitted by egghead(1), visit this page
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This is one of those questions I was never going to get. It's not in FA, I don't think I've seen it in class.

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hungrybox  same :( +
masonkingcobra  My issue was the stem said no skin damage (I would think pulling out your hair damages your scalp) [Turns out it does not](http://onlinelibrary.wiley.com/doi/full/10.1111/j.1529-8019.2008.00165.x) +
gh889  FA 2019, pg 551 +9
meningitis  Compulsively pulling out oneโ€™s own hair. Causes significant distress and persists despite attempts to stop. Presents with areas of thinning hair or baldness on any area of the body, most commonly the scalp. Incidence highest in childhood but spans all ages. Treatment: psychotherapy is first line; medications (eg, clomipramine) may be considered. +15
step1soon  FA 2019 pg 551 +1
teepot123  damn its in FA and Ive never ocne read it XO +


submitted by yo(89), visit this page
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they're talking about a splenorenal shunt procedure

https://my.clevelandclinic.org/health/treatments/4950-distal-splenorenal-shunt

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hungrybox  be honest did u know that before looking it up +9
meningitis  @hungry, because you didn't know it, doesn't mean he didn't. This is a forum for answering questions and helping out, not dissing or showing off. Grow up before becoming a doctor. +32
sympathetikey  Relax @meningitis. Hungry's just messin :) +10
sbryant6  Looks like somebody needs an enema to get that stick out. +1
chandlerbas  ya'll are too TP/(TP+FN) lol +15


submitted by est88(19), visit this page
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Retroperitoneal structures: SAD PUCKER.

Only the descending colon is part of this.

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meningitis  SAD PUCKER: Suprarenal (adrenal) glands [not shown] Aorta and IVC Duodenum (2nd through 4th parts) Pancreas (except tail) Ureters Colon (descending and ascending) Kidneys Esophagus (thoracic portion) Rectum (partially) +25
cienfuegos  I find "SAID PUCKER" to be helpful because it includes IVC +5
lovebug  FA 2019, 354page~ +
realnorthomfs  FA2020, Pg 360 +


submitted by hungrybox(1277), visit this page
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jugular venous distention = left heart failure

pulmonary edema = right heart failure

Four-chamber dilation is the most likely answer.

Other answers:

  • Assymetric septal hypertrophy, myocardial disarray: these are both classic findings in hypertrophic cardiomyopathy (HCM)
  • endocardial fibroelastosis: a rare restrictive cardiomyopathy seen in infants/children
  • lymphocytic infiltration of the myocardium: seen in viral (autoimmune) myocarditis. A cause of dilated cardiomyopathy, but there was no mention of a preceding viral illness.
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meningitis  I think you meant: Jugular venous distention = LT HF Pulmonary edema = RT HF +4
hungrybox  woops yea I meant Jugular venous distention = RIGHT HF, Pulmonary edema = LEFT HF +12
jackie_chan  What threw me off the picking 4-chamber dilatation was it seemed like that would be a major cardiac/ventricular remodeling and the vignette gave a somewhat acute 2 week onset +


submitted by mcl(671), visit this page
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PCOS is associated with abnormal production of sex steroids, including dysfunction of estrogen production and progesterone. Chronically elevated levels of estrogen can cause endometrial hyperplasia.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3917599/

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meningitis  Why isnt it endometriosis? Could someone help me out on this? +2
meningitis  Sorry, I was confusing with higher risk for endometrial carcinoma. +1
vi_capsule  Estrogen is responsible for cyclical bleeding and pain associated with endometriosis hence progestin is a treatment modality. But estrogen isnt a risk factor for Endometriosis. Rather theres retrograde flow, metaplatic transformation etc theories are responsible for endometriosis. +1
sympathetikey  Tfw you get so thrown off by a picture that you don't read the question properly. +34
hyperfukus  @meningitis idk if u still care lol but always go back to endometriosis=ectopic endometrial tissue outside of the uterus so you can rule it out since increased estrogen would cause you to have worsened endometriosis or a thicker one but not directly...you can see the clumps of the follicles in the ovaries if you look super close so that along with the presentation takes you to PCOS and anytime you don't have a baby or stay in the proliferative phase(estrogen phase) you get endometrial proliferation-->hyperplasia--->ultimately carcinoma +2
lovebug  FA 2019, page 631 +1
lovebug  Other answer H)Meigs syndrome : triad of 1) ovarian fibroma, 2) ascites, 3) pleural effusion. โ€œPullingโ€ sensation in groin. FA 2019, pg 632 +1
xw1984  Isn't option G, Leiomyomata uteri, associated with high estrogen level? Per FA 2020, fibroid is estrogen sensitive. +2
ownersucks  @xw1984 gross image would show multiple whorled masses +1


submitted by mcl(671), visit this page
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PCOS is associated with abnormal production of sex steroids, including dysfunction of estrogen production and progesterone. Chronically elevated levels of estrogen can cause endometrial hyperplasia.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3917599/

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meningitis  Why isnt it endometriosis? Could someone help me out on this? +2
meningitis  Sorry, I was confusing with higher risk for endometrial carcinoma. +1
vi_capsule  Estrogen is responsible for cyclical bleeding and pain associated with endometriosis hence progestin is a treatment modality. But estrogen isnt a risk factor for Endometriosis. Rather theres retrograde flow, metaplatic transformation etc theories are responsible for endometriosis. +1
sympathetikey  Tfw you get so thrown off by a picture that you don't read the question properly. +34
hyperfukus  @meningitis idk if u still care lol but always go back to endometriosis=ectopic endometrial tissue outside of the uterus so you can rule it out since increased estrogen would cause you to have worsened endometriosis or a thicker one but not directly...you can see the clumps of the follicles in the ovaries if you look super close so that along with the presentation takes you to PCOS and anytime you don't have a baby or stay in the proliferative phase(estrogen phase) you get endometrial proliferation-->hyperplasia--->ultimately carcinoma +2
lovebug  FA 2019, page 631 +1
lovebug  Other answer H)Meigs syndrome : triad of 1) ovarian fibroma, 2) ascites, 3) pleural effusion. โ€œPullingโ€ sensation in groin. FA 2019, pg 632 +1
xw1984  Isn't option G, Leiomyomata uteri, associated with high estrogen level? Per FA 2020, fibroid is estrogen sensitive. +2
ownersucks  @xw1984 gross image would show multiple whorled masses +1


submitted by neonem(630), visit this page
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This is a case of porphyria cutanea tarda. The way I remember this is that it's the only high-yield porphyria that has skin manifestations due to UV. I remember this by "After U (uroporphyrin), it's UV". Apparently it's also associated with Hepatitis C, which could be the reason why there's increased AST & ALT, or it could be due to toxic buildup of intermediates in heme synthesis.

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meningitis  Why cant it be protoporphyrinogen oxidase? It was because of that reason (Increased AST and ALT) I thought it wasnt uroporphyrinogen decarb. My train of thought was: "wow, mitochondria are messed up.. there must be a lot of intermediates in there,therefore the Uroporph decarb must OK." +
arlenieeweenie  FA 2019 pg. 417, the later on the defect in the heme synthesis pathway is the one more associated with skin findings! Also according to this year's edition uroporphyrinogen synthase is now known as prophobilinogen deaminase +9
nobody  AMBOSS has estrogen therapy listed as a susceptibility factor for PCT. I could not find a link between elevated AST/ALT and estrogen therapy that would occur 15 years into treatment. +


submitted by taway(35), visit this page
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Does anybody understand why we are allowed to interfere with the clinical decisionmaking of two other specialists directly? Wouldn't that muddy the waters even more by adding our opinion? I don't see the underlying principle that explains the rationale in this answer.

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jcrll  I think it's about adding our opinion and more about seeing what the situation is because a patient contacted you in distress. The others are about contacting management off hearsay; that could also "muddy the waters," I Is this question also addressing quaternary prevention? +3
meningitis  I agree with jcrll. My same thought process but then I changed it to psychiatric consultation in order to first attend the patient's distress and anxiety since it was hindering her decision making. Besides, the whole ordeal about her treatments and ineffectiveness was emotionally and physically exhausting her. +4
vi_capsule  Referral is NEVER a answer +12
tsl19  Going straight to the chair of the ethics committee without having spoken to the other physicians would be inappropriate because it would be jumping a bunch of steps in communication first - like jcrll said, you want to get the picture of what's going on from the other physicians first. Maybe the gynecologic oncologist isn't actually as opposed to palliative measures as the patient perceives him to be and thinks he's doing what the patient wants, etc. It could just be miscommunication, which you could help clear up without getting ethics involved ... better to start there. +12
an_improved_me  Also, to add a little bit: internists on a healthcare team are the care coordinators. For any given problem a patient has, the internist is responsible for managing all the different aspects of a patients treatment. In this case, the intern has to manage the dissenting opinions of her different gynecologists. In other instances, an internist may have to manage the disagreement between a Surgeon vs. IR vs. Onc. +2


submitted by nosancuck(102), visit this page
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Yo dis B got NO INTERNAL FEMALE ORGANS

Why dat!???

We be lookin at someone with an SRY from dere Y chromie! Dey be a Y chromie Homie so they be makin some Testis Determinin Factor which I be sure makes some nice lil ANTI MULLERIAN FACTOR so dey aint got that Female Internal Tract u know what i be sayin

And since wimminz is da DEFAULT they stil be gettin dose pussy lips and breastes

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meningitis  The above explanation is correct (disregarding the hard to read and unprofessional dialect) but just in case anyone was wondering: chromatin-negative= Just a quick way of knowing it was a boy. The term applies to the nuclei of cells in normal males as well as those in individuals with certain chromosomal abnormalities +17
yotsubato  Turner syndrome patients are also chromatin negative as well though.... +6
sympathetikey  I didn't know a complication post-meningitis was lack of humor. +6
sympathetikey  Ah, didn't read the last line. Yeah, that is taking it a bit far +32
niboonsh  yall are haters. this is the first explanation that has ever made sense to me +7
arkmoses  https://www.youtube.com/watch?v=yuXL-3eoB-o&t=77s Interesting syndrome watching this helped me to put it into real life perspective, interesting points they have no pubic hair/body hair, they apparently also dont smell, and breast size is usually increased... +2
whoissaad  How does chormatin-negative indicate a normal cell? Isn't chormatin just condensed DNA? +2
cienfuegos  According to this paper most individuals with Turner Syndrome are chromatin negative: "One of the initial laboratory procedures used to confirm or rule out this diagnosis involves a sex chromatin determination from a buccal smear. Cells from the lining of the mouth are stained for the presence or absence of X-chromatin or Barr bodies, which represent a portion of an inactivated X chromosome. The typical Turnerโ€™s syndrome patient, who has 45 chromosomes and only one sex chromosome (an X), has no Barr bodies and is, therefore, X-chromatin negative. This abnormal X-chromatin negative finding in the majority of Turnerโ€™s syndrome females is similar to the result found in a normal male, who also has only one X chromosome, and differs from the X-chromatin positive condition observed in the normal female, who has two X chromosomes. Occasionally, the patient with features of Turnerโ€™s syndrome is found to be X-chromatin positive." https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6233891/ +2
hyperfukus  i really hate haters this is awesome! +2
selectuw  to add to the above, free testosterone is aromatized to estrogen leading to breast development +1
misrao  Is the free testosterone not creating male internal or external gentalia because of the defect in androgen receptors? +1


submitted by hungrybox(1277), visit this page
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Hydrochlorothiazide is a thiazide diuretic => thiazide diuretics are associated with hypokalemia.

What other diuretics are associated with hypokalemia? Loop diuretics.

Why?

Inhibition of Na+ reabsorption occurs in both loop diuretics (inhibit NKCC cotransporter) and thiazide diuretics (inhibit NaCl cortransporter). All of this increased Na+ increases Aldosterone activity.

Relevant to this problem, Aldosterone upregulates expression of the Na+/K+ ATP antiporter (reabsorb Na+ into body, expel K+ into lumen). This results in hypokalemia in the body.

Hang on, there's more high yield info!

Aldosterone does one other important thing - activation of a H+ channel that expels H+ into the lumen.

So, given that this patient has hypokalemia, you know there is upregulation of Aldosterone. Do you think her pH would be high, or low? Exactly, it would be high because inc. Aldosterone => inc. H+ expelled into the lumen => metabolic akalosis.

Now you understand why both loop diuretics and thiazide diuretics can cause what's called "hypokalemic metabolic alkalosis."

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hungrybox  jesus this answer was probably too long i'm sorry +9
meningitis  I disagree. It's the complete thought process needed for many Thiazide/Loop question that can be thrown. Thanks. +17
amirmullick3  This is what NBME should be providing with each question's correct answer! Thanks hungrybox! +1
amirmullick3  @hungrybox did you mean "All of this DECREASED Na increases aldosterone activity."? +2
pg32  Anyone care to explain why she feels she has, "lost [her] pep"? Is that due to the hypokalemia? Or hypercalcemia caused by the thiazides? +
cmun777  @madojo @pg32 I assumed between her hypokalemia (which can cause weakness/fatigue) and possible contraction alkalosis those were the most likely causes for the "lost her pep" comment. I think if they wanted to indicate hypercalcemia to differentiate if loop diuretics were also in the answer choices they would certainly give more context for hypercalcemia sx +


submitted by neonem(630), visit this page
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Obstructive uropathy causes a postrenal azotemia --> when prolonged, tubular damage ensues. This leads to an acute tubular necrosis, characterized by necrotic plugs in the tubular system as seen in the image

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meningitis  Does anyone know the relevance of the stem saying: "during this time she also has been crying frequently"? +53
usmleuser007  Think the postrenal azotemia is d/t her pregnancy. With the increasing in size fetus, the pelvic cavity is being compressed and thus there is pressure on the ureters. This leading to the presentation. As per above --- the crying maybe just d/t her pain and emotional stress caused by worrying about possible complications regarding her fetus. +4
maxillarythirdmolar  My gut tells me it must be some sort of transient change in placental size with hormonal changes. It's reminiscent of what you might expect for breast changes during the menstrual cycle, imo +
j44n  or maybe the fetus is literally crushing her ureters into the wall of her pelvis and shes got an infected kidney +4


submitted by hayayah(1212), visit this page
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Iron overdose is a cause of a high anion gap metabolic acidosis.

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meningitis  I found this to add a little bit more explanation as to how it causes the acidosis if anyone needs it. 1. Mitochondrial toxicity - decreases aerobic respiration and shunts to lactic acid production 2. Cardio toxicity (Secondary to Mitochondrial toxicity) leads to cardiogenic shock (hypoperfusion), which causes lactic acidosis 3. Hepatotoxicity - Decreases lactate metabolism, causing lactic acidosis 4. When in trivalent form (Fe+3), it can react with 3 molecules of H2O --> FeOH3 + 3H+ This will then deplete Bicarb buffering system resulting in non-gap acidosis. Source: https://forums.studentdoctor.net/threads/iron-poisoning-anion-gap-or-non-anion-gap-acidosis.958285/ +20
sympathetikey  None of the other choices were even metabolic acidosis. They threw us a bone with this one. +33
imnotarobotbut  Don't changes in bicarb take a few days? How did his bicarb drop down to 8 in 12 hours? +2
charcot_bouchard  its met acidsis. not compensation +9
j44n  they did throw us a bone however I didnt catch it +7


submitted by hayayah(1212), visit this page
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Most restriction enzymes bind palindromes.

So both 5'CCGG or 3'GGCC would have been acceptable in this scenario.

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meningitis  Yes, correct. The 5'GGCC option could cause some confusion. +1
guillo12  I really don't understand the question nor the answer. Can someone explain it for dummies like me? +16
whossayin  yes please.. I'm with guillo12 on this +
sugaplum  @guillo12 @whossayin questions says you've created a new cut site, 1. look at the region on the sick vs healthy. The C to G is the change 2. Write out the sick "CCGG" from 5'3'- you could write out the whole thing, but the answer only has 4 letters, so being lazy here 3. write under it, its complement, the dna base pair. So "GGCC" 4. remember both strands are going in opposite directions when you write them out on top of each other. 5. So the bottom strand actually reads 5' CCGG 3' so that is the answer I hope that clears it up +60
shirafune  To add to the palindrome part, many restriction endonucleases actually function as dimers. Each individual subunit usually has a nickase, so to create a double-stranded break in DNA, they must bind a palindrome so that each enzymatic domain creates a single-stranded break (thus a double-stranded break). +1
alimd  Why do we start from CCGG? Why not CGGG or TACC? +6
alimd  Why do we start from CCGG? Why not CGGG or TACC? +1
ssbhatti  I think its due to the palindrome requirement? +
bbr  Maybe I'm missing a part here, but the substrate that the enzyme will bind to will be the DNA. I went with the line that was from the questions stem, as it is the mtuated DNA will be recognized by the restriction enzyme. I didnt see the need to convert it into base pairing. Let me know what you guys think. +2
uloveboobs  @bbr I agree. I'm definitely not an expert in these lab tests, but the question asks "substrate specificity." I was thinking that it would recognize the abnormal DNA; nothing to do with RNA. I didn't know about the palindromic preference of restriction enzymes, but I don't think there's any need to figure out base-pairing and whatnot here. (At least for this question it didn't work out that way!) +
spaceboy98  sugaplum, I'd give you an award if this was Reddit +6


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