welcome redditors!to snoo-finity ... and beyond!
Welcome to mcl's page.
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Comments ...

 +0  (nbme24#18)

lolol so instead of using fomepizole they just gonna get him real drunk

johnson  yep - supposedly, ethanol is used when a hospital/facility doesn't have fomepizole.

 +1  (nbme24#4)

Bonus cadaver diagram, idk why this was on pinterest...........?

yotsubato  nurses

 +3  (nbme23#10)

So if you didn't h8 bedbugs enough, they can apparently also serve as vectors for drug-resistant bacteria including MRSA HOW FUN IS THAT

spacepogie  SO FUN

 +2  (nbme23#23)

To expand on this, what we think happens with Parkinson's disease (and parkinsonianism) is an imbalance between dopamine and acetylcholine. It makes more sense if you look at this diagram, paying particular attention to the indirect pathway. Loss of dopaminergic (DA) neurons from the substantia nigra (SNc) results in constant activation of those ACh secreting neurons, which ultimately results in inhibition of thalamus from initiating movements. Therefore, using anticholinergics help with parkinsonianism secondary to haldol.

mcl  Also, you don't wanna use sinemet since that would be counterproductive

 +4  (nbme23#16)

In case you wanna go super nerd and read about myelin, capacitance, and resistance, this guy does a good job.

nwinkelmann  This really helped me, at least the pictures did. Here's my interpretation of the pictures in not super scientific terms: capacitance is like the "capaciy" to keep ions close to the membrane. Myelin puts a barrier between the ions in the conductive environment (ECF or ICF) and the nerve membrane. The higher the capacitance, the closer the ions are to the membrane, so it's like the charge effect is "more potent" so harder to change the membrane potentia, whereas if the ions are farther from the membrane, the charge effect is "less potent" so easier to change the membrane potential and thus easier to depolarize. Thus, with myelin, there is decreased capacity of the ions to be close to the membrane, so in demyelinating conditions, the ions can be really close to the membrane, i.e. higher capacitance.
sweetmed  this helped a lot!
roaaaj  Well explained!

 +3  (nbme23#40)

FA 2019 P 573 - The only part of the nephron that first aid says has an effect on PO4 3- is PCT.


 +3  (nbme23#10)

This is a nice quick refresher of what AUC is.



 +2  (nbme23#18)

According to this paper, insulin inhibits alpha cells from releasing glucagon. This is the relevant figure from the paper.

medpsychosis  There are three ways that Glucagon secretion is stimulated: +(1) a stimulatory effect of low glucose directly on the alpha cell, +(2) withdrawal of an inhibitory effect of adjacent beta cells, and +(3) a stimulatory effect of autonomic activation. The response of Glucagon to hypoglycemia is diminished in T1Diabetes. Hence in this pt, the impaired release of Glucagon allows for prolonged Hypoglycemia. Reference: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3005043/

 +7  (nbme23#26)

Patient with bilateral renal artery bruits and hypertension will for sure have activation of RAS system and therefore increase in angiotensin.

Although pheochromocytoma and consequent elevated catecholamines can increase blood pressure, symptoms are typically episodic and renal bruits are not likely to be heard. Elevated levels of serotonin can also cause hypertension, but we would also expect to see flushing; also, there is nothing in the stem to indicate patient is taking SSRIs or something else that could predispose her to elevated levels of serotonin. Elevated levels of thyroid hormone could also give patient hypertension, but we would also expect other signs of hyperthyroidism (tremors, weight loss, etc.).

I was a little confused if EPO would be elevated -- if there is stenosis of renal arteries (as indicated by the bruits) the kidneys could also detect this as hypoxia and ramp up production of EPO. However, I ended up going with angiotensin since it seemed more "concrete" to me that RAS would be up. Does anyone know why it's not EPO?

brise  Wouldn't that be more long term?
sugaplum  I think Epo would indicate Rcc or renal failure, she seems like she has "just" refractory HTN, and no other sx to indicate anemia.
davidw  She has Fibromuscular dysplasia which should be in your differential for a young female with hypertension ( along with Conns syndrome and pheochromocytoma). it typically causes stenosis and aneurism formation of the renal arteries leading to elevated renin.

 +4  (nbme23#34)

To expand on this, organophosphates are commonly used as insecticides, and function by binding acetylcholinesterase and "deactivating" it, so to speak. This results in an excess of ACh within the synapse, which causes sludge syndrome (vomiting, sweating, diarrhea -- basically lots of fluids). The treatment for this is typically atropine (antimuscarininic), and pralidoxime (if given early enough, can "reactivate" the ACh-ases). The diagram given does not show ACh-ase, only the ACh-R, therefore D is the best answer.


 +4  (nbme23#10)

This figure is a helpful refresher for the 68/95/99.7 rule


 +13  (nbme22#37)

This image is useful. Note that the stain used makes myelin appear dark.

Vignette is typical for Parkinson's disease. Area D is the substantia nigra.

oznefu  Oh nice! Thanks!

 +0  (nbme22#19)

Ewing sarcoma is the second most common bone malignancy in children. Histology is usually described as a small cell tumor with high N:C ratio.

praderwilli  Also the concentric layers of reactive bone sounded like "onion skin" to me!

 +0  (nbme22#8)

Homegirl got some cervical outlet syndrome and should probably take some stuff out of her backpack or get one of those lil roller ones.

mcl  Whoops, my bad, THORACIC outlet syndrome
dr.xx  Stretching, occupational and physical therapy are common non-invasive approaches used in the treatment of TOS. The cervical rib can be surgically removed.

 +1  (nbme22#29)

These images are useful in combination.


 +4  (nbme22#39)

Poison ivy triggers a type IV hypersensitivity (mediated by T cells); only one of the answer choices mentions T cells.


 +0  (nbme22#44)

Scabies likes to burrow in the areas between the fingers and toes (FA 2019 161) and causes itching. Could also potentially be lice (groin involvement), but treatment for either overlaps -- gotta use permethrin.

kchakhabar  If only one person is there to see the doctor, why would the doctor prescribe medicine even for his family members who are not there?
mcl  Unfortunately, both of these are pretty contagious conditions. FA mentions that scabies spreads via skin to skin contact, and goes on to mention that you're supposed to treat close contacts. I think in this scenario it's ok to give permethrin to the family members who are not present but affected (it's also non-prescription in some cases, I believe.) Slightly related note, similar to why you would treat the sexual partner of someone with chlamydia/gonorrhea, or close contacts of someone with n. meningitides infection.

 +2  (nbme22#45)

To expand on this, pathologyoutlines describes the histology of kapowsi sarcoma as "spindle cells forming slits with extravasated red blood cells"

mcl  lul i don't know why i spell kaposi like that, my b
bubbles  This site is super helpful. Thanks for sharing :)
mcl  yesssssss ofc <3 I love path outlines
usmleuser007  Just realize that spindle cells are similar to the endothelial cells of blood vessels. Anything that have vessel association might have spindle-shaped cells. a. NF-1 b. NF-2 ~ Schwannoma (Antoni A) = Cutaneous neurofibroma ~ high cellularity (w/ palisading patterns with interspersing nuclear-free zones called Verocay bodies c. Leiomyoma (uterus & esophagus) d. Mesothelioma (cytokeratin positive) e. Anaplastic Thyroid cancer (biphasic & along with giant cells) f. Medullary Thyroid cancer (can also have polygonal cells) g. Primary cardiac angiosarcoma (malignant vascular spindle cells) h. Osteosarcoma (bone cancer) (pleomorphic cells) i. Meningioma j. Kaposi's Sarcoma (HHV-8) = Slit-like vascular spaces with plump spindle-shaped stromal cells

 +1  (nbme22#37)

Beta-2 receptors are coupled to Gs proteins, which activate adenylyl cyclase and increase cAMP. Cyclic AMP then increases activity of protein kinase A, which phosphorylates myosin light chain kinase, ultimately resulting in smooth muscle relaxation. Albuterol, a B2 agonist, is therefore useful in treating bronchospasm.

impostersyndromel1000  are you able to clarify that phosphorylated myosin light chain kinase from cAMP/PKA and dephosphorylated myosin light chain from cGMP both cause smooth muscle relaxation? saw this on another Q with the nitrates causing headache so now im confused
dubywow  @impostersyndromel1000: Here is an image that summarizes cAMP and cGMP actions in smooth muscle cell very will. Hope it helps. link

 +1  (nbme22#28)

CDC recommended treatment of schistosoma mansoni is praziquantel.


 +2  (nbme22#8)

Since you're losing all your bicarb into your pee, you would expect the pH to be more alkaline. Also, since there is decreased Na+/H+ antiport, there is less sodium reabsorbed and therefore increased loss of free fluid to the urine.

mcl  useful figure http://users.atw.hu/blp6/BLP6/HTML/common/M9780323045827-036-f002.jpg
joker4eva76  Why wouldn't this be similar to a Type 2 RTA where urinary pH <5.5?
mcl  I can't remember exactly what the question was asking off the top of my head, I think it was asking about relative to normal? But I think you're right in that the alpha intercalated cells (AIC) can still dump H+ into the urine and acidify it to an extent. And, like in RTA2, I don't know that the action of the AIC would be able to overcome the bicarb and acidify the urine enough for it to be the usual pH, so the urine should still be more alkaline compared to baseline. Kinda sucks, pH less than 5.5 should technically be acidic but it's alkaline for pee.
mcl  JK, normal urine pH is around 4-8, but I guess they consider closer to 5.5 on the more alkaline side...? I guess I would go more off that the alpha intercalated cells can't completely compensate for the amount of bicarb in the pee due to the CA inhibitor, not so much the actual pH.
meningitis  Anhydrase inhibitors also affect the anhydrase inhibitors that are used in the AIC in order to excrete the H+. Here is a link:**http://pedclerk.bsd.uchicago.edu/sites/pedclerk.uchicago.edu/files/uploads/distal_0.png**
mcl  ohhhhhhhhhhhhhhhhhhhhhhh my god duh yes thank you <3
meningitis  Lol yw!!

 +1  (nbme22#32)

Patient likely has PCOS. PCOS is associated with elevated levels of LH from the pituitary, which stimulates ovaries to produce increased amounts of sex steroids (including androgens --> hirsutisim). Androstenedione is converted to estrone in adipocytes, which results in still further increased release of LH. Obesity and insulin resistance is associated with PCOS.


 +9  (nbme22#30)

The question is referring to the hexosamine pathway.

Carbamoyl phosphate and arginine are involved in the urea cycle. So is n-acetylglutamate (NAG) (regulates production of carbamoyl phosphate).


 +9  (nbme22#22)

Despite a numeric value (blood pressure) being measured, patients would be designated either hypertensive or normotensive. To my understanding, the best test for comparing categorical variables across groups is a chi square test.

In contrast, a t-test is used to compare between the means of two groups (measured variable must be quantitative).


 +0  (nbme22#47)

page 119 FA Patient is presenting months after the transplant, which means it can't be hyperacute unless he stopped taking his immunosuppressants. Acute/chronic/GVH disease are mediated by T cells for the most part (I think), so this would mean lymphocytic infiltrates.

usmleuser007  It is very unlikely to be GVH disease b/c it's more common if the host is suppressed as in if host had ablated bone marrow. (FA states that it's more common with bone marrow & liver transplants)
usmleuser007  any one care to explain why fibrous scars with plasma cells not a good option?...

 +1  (nbme22#1)

Pronator teres and quadratus are both supplied by median nerve (C5/C6/C7/C8/T1, so that's not super helpful.) Extension of the forearm is radial nerve (also C5-T1, also not helpful). This does tell us is it can't be isolated median or radial. Triceps tendon reflex is C7/C8, which narrows it down to these two.

Can anyone explain why it's C7 over C8?

joha961  Same question. How could you determine between the specific nerve roots (C7 vs. C8)?
mcl  Someone I was talking to (and post below) was saying that first aid mentions triceps is C7, so that's what should've been the big thing for us.

 +4  (nbme22#15)

To expand on this, contraction of flexor digitorum profundus muscle results in flexion at the DIPs and PIPs. The tendon attaches at the tip of the finger, in contrast to flexor digitorum superficialis (attaches at the PIPs). Recall innervation of the forearm muscles is mostly from the median nerve, except for 1.5 muscles (ulnar half of flexor digitorum profundus and the flexor carpi ulnaris, both supplied by ulnar which makes it ez to remember yay).

But also if you got this wrong like me go read that link because it's a really nice review.


 +5  (nbme22#14)

Intercostal veins drain into the azygous/hemiazygous veins, which run right next to the vertebral column. Another useful diagram showing left and right intercostal veins.


 +0  (nbme21#30)

Per p608 in FA 2019, SRY on Y chromosome results in development of testes. DHT results in development of male external genitalia (and the prostate).

mrsmac  No sertoli cells or lack of mullerian inhibitory factor makes more sense. bc there is both male and female internal genitalia but only male external genatalia. and karyotype would show 46XY. First Aid 2018 pg. 604 - the "Sexual Differentiation" charge delineates exactly this. If it were 5areductase deficiency the child would have testicles and scrotum, which in this case is absence. Hope this makes sense. Please let me know if you disagree and why. Thanks.
mixmasta  I believe the tricky part is that they don't mention the status of the Male external genitalia. Pg. 605 from FA ( bottom portion) shows the external development of the Male/Female genitalia; you see DHT is need for male. Furthermore, pg. 604 (SEXUAL DIFFERENTIATION) DHT is also needed for Male external development.
niboonsh  My understanding of this is that the diagnosis is 5alpha reductase deficiency because the newborn has female external (aka ambiguous) with male internal (aka "male genital ducts"). According to FA, leydig cells produce testosterone, which can either stimulate the mesonephric duct to form the INTERNAL male genitals (as see in the pt). Testosterone can also be acted on by 5alpha reductase to become Dihydrotestosterone, which forms the male EXTERNAL genitalia. Since this kid has "female" genitals, but has male insides and is 46XY, id say this is a simple case of 5alpha reductase deficiency. No sertoli cells or no MIF would present as both female and male internal (because MIF typically inhibits differentiation of female internal) and male external genitalia (bcuz leydig cells are unaffected)

hyperfukus  this link is great! they're still kind of close together :( its so hard to tell for me w/o reference of the others
hyperfukus  this link is great! they're still kind of close together :( its so hard to tell for me w/o reference of the others

 +8  (nbme21#36)

This image is very helpful.

seagull  http://www.siumed.edu/~dking2/erg/GI178b.htm Another histology slide with labels
masonkingcobra  I like to think that the parietal cells look like "fried eggs" classically

 -2  (nbme21#17)

Methionine is an essential amino acid. All others listed are not.

scalpelofthenorth  Pg 81 Tyrosine is listed as an essential AA. Should be tryptophan for those who got this wrong like me.
neonem  But tyrosine can come from phenylalanine, so it's not really essential right?
gh889  in FA2019, it is listed as Tryptophan, not Tyrosine. That was corrected.
usmleuser007  Note: Tyrosine is ONLY essential with PKU in children
niboonsh  bro FA2018 lists tyrosine as an essential AA. They played us.

 +6  (nbme21#19)

Patient may have hereditary angioedema, which is associated with "recurrent attacks of intense, massive, localized subcutaneous edema involving the extremities, genitalia, face, or trunk, or submucosal edema of upper airway or bowels". The article goes on to say "C1-esterase inhibitor works directly on the complement and contact plasma cascades to reduce bradykinin release" which is also probably good to know.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3666183/

notadoctor  Thought this was a trick question as C1 esterase deficiency also results in a decrease in C4. However, the second answer choice was not referring to C4 but to C4 binding protein, which I now know is different. I also didn't realize C1 esterase was technically a complement protein.
youssefa  Based on many sources hereditary angioedema does NOT cause a rash (urticaria) which is a main differentiating point between angioedema and allergy. This mislead me in this question. Any clarification?
ergogenic22  +1 on the above because uptodate states that c1 esterase inhibitor deficiency, both acquired and nonhereditary, are both non-urticarial, non-pruritic, and that is confirmed by the above linked article
sahusema  Question writer probably didn't know the difference between cutaneous urticaria and subcutaneous edema.

 +2  (nbme21#12)

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/

meningitis  Why isnt it endometriosis? Could someone help me out on this?
meningitis  Sorry, I was confusing with higher risk for endometrial carcinoma.
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.
sympathetikey  Tfw you get so thrown off by a picture that you don't read the question properly.
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

 +9  (nbme21#45)

Not sure if this is the right way to think about it, but if PT and PTT are both prolonged, this most likely means there is a problem with the common pathway (aka factor X).

temmy  exactly...i just thought the problem has to be where they meet or somewhere similar to both..hence the common pathway 12(PTT Heparin) 7 (PT, Warfarin) 11 9 10 5 2 1 In my head, both sides are looking for the perfect 10

 +2  (nbme21#9)

When working on acid/base disorders, it helps to look systematically at the following: (1) pH (which sadly was not given in this problem), (2) figure out which problem is primary by looking at PaCO2 and bicarb, and (3) look for any compensation (which the question doesn't ask but still).

Here, we see that the CO2 is high on the ABG. This means that patient is hypoventilating since levels of CO2 are ventilation dependent, and also that patient has respiratory acidosis. Also, bicarb is low, which implies that it's being "soaked up" by metabolic acidosis.

privatejoker  I just look at these as "what makes the most sense" and this is is sufficient in nearly every scenario. Out of the given options, the only explanation that even lines up with the given numbers is the answer choice.

 +8  (nbme21#30)

This is a pretty good figure showing the conversion of membrane phospholipids to arachidonic acid/leukotrienes etc.

Blockade of COX enzyme by ibuprofen results in decreased production of prostaglandins H2 and E2, while causing the precursors to "back up" (increased arachidonic acid). This, in turn, results in increased production of leukotrienes.


 +2  (nbme21#30)

Deltoid is innervated by axillary nerve, which comes from roots C5/C6. Actions of the deltoid include abduction of the upper extremity.

seagull  I hope everyone memorized every single part of the brachial plexus and all the roots of each, No detail let untouched!!!
mcl  In case anyone else has purged the whole brachial plexus from your memory (like me), this is a great resource linked by another user. https://geekymedics.com/nerve-supply-to-the-upper-limb/

 +4  (nbme21#13)

Niacin (vitamin B3) antagonizes VLDL cholesterol secretion

sbryant6  Fibrates stimulate PPAR-alpha --> LPL upregulation --> decreased triglycerides. However, this question asked about a vitamin. Vitamin B3=niacin.

 +1  (nbme21#1)

Page 250 FA - Ethambutol is associated with visual disturbances (changes in color vision).

rocmed  Ethambutol is associated with optic neuritis which can cause loss of visual acuity and red-green color blindness
dashou19  On FA page 250, it is said that Isoniazid can also cause optic neuritis and color vision change. Sometimes it hurts if you know too much lol

 +4  (nbme21#44)

While antihistamines with action at H1 receptors are used for allergies, H2 antihistamines are typically used for ulcers. Therefore the best answer is stabilization of mast cell membranes. These drugs (cromolyn) prevent vesicles of histamine from fusing with the membrane.


 +4  (nbme21#14)

Vibrio cholerae is a gram-negative, comma shaped bacteria that can cause watery diarrhea. Cholera toxin functions by activating the Gs proteins --> increasing activity of adenylyl cyclase --> increased cAMP --> increased Na+ and Cl- efflux --> diarrhea.


 +3  (nbme21#34)

Membranous glomerulopephritis (aka membranous nephropathy, p 584 FA 2019) may occur secondary to drugs such as penicillamine. Immunofluorescence shows granular deposits due to immune complex deposition. Will also see diffuse capillary and GBM thickening, and SEM will show spike and dome appearance due to subepithelial deposits.


 +0  (nbme21#44)

Furosemide and other loop diuretics are indicated for use in volume overload secondary to renal failure. Recall loop diuretics inhibit the Na+/K+/Cl- pump at the thick ascending loop of Henle, which messes with the hypertonicity of the medulla and therefore prevents urine from being concentrated. This results in increased fluid loss to urine, and is helpful in treating symptoms of edema.


 +5  (nbme21#7)

Gait problems raises suspicion for alcohol abuse or inhaled glue. However, onset of gait problems is relatively rapid (couple of months) and gait disturbance with regards to alcohol is either due to intoxication or chronic abuse. Alternative explanation available on SDN. Also see toluene toxicity on medscape.

sbryant6  I got this correct solely based on the patients demographic. Glue is cheap and easily accessible to underage populations.
whossayin  Kinda racist of us but that’s how I reasoned my answer too lol @sbryant6
hpsbwz  how is it racist if the only thing thats given is his age lol @whossayin

 +2  (nbme21#2)

Patient most likely has Tay-Sachs disease. This figure nicely shows the biochemical pathway. Recall that both Tay-Sachs and Neimann Pick disease present with a cherry red spot on fundoscopy, but Tay Sachs lacks the hepatosplenomegaly seen in NP.

hungrybox  Man this is such a nice figure except it doesn't have Krabbe disease :(
mcl  Here's another one with Krabbe! :) https://epomedicine.com/wp-content/uploads/2017/01/lysosomal-storage-diseases-enzyme-defects.jpg
hungrybox  thank u
kjfhewiufh  [special]

 +1  (nbme21#46)

Other way to get this question is by eliminating other options -- this figure is useful in listing some mutations and associated cancers.


 +1  (nbme21#33)

"chronic high oxygen saturations can adversely affect lung and eye outcomes of preterm infants." link





Subcomments ...

submitted by usmleuser007(126),

my list of spindle type cells and conditions:

  • a. NF-1
  • b. NF-2 ~ Schwannoma (Antoni A) = Cutaneous neurofibroma ~ high cellularity (w/ palisading patterns with interspersing nuclear-free zones called Verocay bodies
  • c. Leiomyoma (uterus & esophagus)
  • d. Mesothelioma (cytokeratin positive)
  • e. Anaplastic Thyroid cancer (biphasic & along with giant cells)
  • f. Medullary Thyroid cancer (can also have polygonal cells)
  • g. Primary cardiac angiosarcoma (malignant vascular spindle cells)
  • h. Osteosarcoma (bone cancer) (pleomorphic cells)
  • i. Meningioma
  • j. Kaposi's Sarcoma (HHV-8) = Slit-like vascular spaces with plump spindle-shaped stromal cells
drdoom  @usmleuser007 to make lists display correctly, try using the plus sign (+) for each "bullet point"; that should work +  
mcl  I love this and I love you +1  
usmleuser007  LOL thanks, had to ddo a lot of digging since "spindle cells" are commonly tested +  


Why is it not ovarian follicle cells? I thought the female analog of Sertoli and Leydig is theca/granulosa cells.

colonelred_  Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen. +2  
brethren_md  Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen +1  
sympathetikey  Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen +1  
s1q3t3  Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen +1  
masonkingcobra  Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen +  
mcl  Wait, but did anyone mention that females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen??? +10  
mcl  But seriously though, pathology outlines says sertoli-leydig tumor "may be suspected clinically in a young patient presenting with a combination of virilization, elevated testosterone levels and ovarian / pelvic mass on imaging studies." As for follicle cell tumors, granulosa cell tumors usually occur in adults and would cause elevated levels of estrogens. Theca cell tumor would also primarily produce estrogens. Putting the links at the end since idk if they're gonna turn out right lol Link pathology outlines for sertoli leydig granulosa cell tumor theca cell tumor +6  
bigjimbo  LOL +  
fallenistand  Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen. +2  
medpsychosis  So after doing some intense research, UPtoDate, PubMed, an intense literature review on the topic I have come to the final conclusion that...... ...... ...... ...... Wait for it.... ..... ..... Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen. +3  
charcot_bouchard  Hello, i just want to add that Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen +1  
giggidy  Hold up, so I'm confused - I read all the posts above but I still am unsure - are sertoli-leydig cells notorious for producing androgen? +1  
subclaviansteele  Hold the phone.....Females can get sertoli leydig cell tumors which are notorious for producing androgen? TIL TL;DR - Females can get sertoli leydig cell tumors = high androgens +  
cinnapie  I just found a recent study on PubMed saying "Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen" +  
youssefa  Hahahahaha ya'll just bored +2  
water  Bored? you wouldn't think so if you knew that females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen +  
nbmehelp  I dont get it +  
redvelvet  how don't you get it that females can get Sertoli Leydig cell tumors, which are notorious for producing lots of androgen? +  
drmomo  what if this means..... females can get Sertoli Leydig cell tumors, which are notorious for producing lots of androgen +  
sunshinesweetheart  hahahaha this made my day #futurephysicians #lowkeyidiots +  
sunshinesweetheart  @medstruggle look up placental aromatase deficiency (p. 625 FA 2019), it would have a different presentation +  
deathbystep1  i am sure i would ace STEP 1 if i only knew that females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen +  
noplanb  Wait... I might actually never forget this now lol +  


Why is it not ovarian follicle cells? I thought the female analog of Sertoli and Leydig is theca/granulosa cells.

colonelred_  Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen. +2  
brethren_md  Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen +1  
sympathetikey  Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen +1  
s1q3t3  Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen +1  
masonkingcobra  Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen +  
mcl  Wait, but did anyone mention that females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen??? +10  
mcl  But seriously though, pathology outlines says sertoli-leydig tumor "may be suspected clinically in a young patient presenting with a combination of virilization, elevated testosterone levels and ovarian / pelvic mass on imaging studies." As for follicle cell tumors, granulosa cell tumors usually occur in adults and would cause elevated levels of estrogens. Theca cell tumor would also primarily produce estrogens. Putting the links at the end since idk if they're gonna turn out right lol Link pathology outlines for sertoli leydig granulosa cell tumor theca cell tumor +6  
bigjimbo  LOL +  
fallenistand  Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen. +2  
medpsychosis  So after doing some intense research, UPtoDate, PubMed, an intense literature review on the topic I have come to the final conclusion that...... ...... ...... ...... Wait for it.... ..... ..... Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen. +3  
charcot_bouchard  Hello, i just want to add that Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen +1  
giggidy  Hold up, so I'm confused - I read all the posts above but I still am unsure - are sertoli-leydig cells notorious for producing androgen? +1  
subclaviansteele  Hold the phone.....Females can get sertoli leydig cell tumors which are notorious for producing androgen? TIL TL;DR - Females can get sertoli leydig cell tumors = high androgens +  
cinnapie  I just found a recent study on PubMed saying "Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen" +  
youssefa  Hahahahaha ya'll just bored +2  
water  Bored? you wouldn't think so if you knew that females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen +  
nbmehelp  I dont get it +  
redvelvet  how don't you get it that females can get Sertoli Leydig cell tumors, which are notorious for producing lots of androgen? +  
drmomo  what if this means..... females can get Sertoli Leydig cell tumors, which are notorious for producing lots of androgen +  
sunshinesweetheart  hahahaha this made my day #futurephysicians #lowkeyidiots +  
sunshinesweetheart  @medstruggle look up placental aromatase deficiency (p. 625 FA 2019), it would have a different presentation +  
deathbystep1  i am sure i would ace STEP 1 if i only knew that females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen +  
noplanb  Wait... I might actually never forget this now lol +  


Why are the IMA and SMA most likely to be affected in her condition?

sattanki  Again, not too sure, but I think they were describing a patient with chronic intestinal angina, which is classically from atherosclerosis of the IMA/SMA. +1  
mcl  I was also thinking about which areas have crappy blood supply (watershed areas), which I assume would be worse off in the case of chronic mesenteric ischemia. If you look on page 357 of FA 2019, SMA & IMA at the splenic flexure is a watershed area; the other is rectosigmoid junction (sigmoid branch from IMA and superior rectal). +  


Why is alternative splicing or post-transcriptional modification incorrect?

tea-cats-biscuits  You just have to know that POMC is a pro-protein that must be cleaved; not sure if there’s anything in the stem that would really have given it away. +  
mcl  Dunno if this helps, but it says "this protein" (singular) is the precursor of two different protein products. This must mean that the modification occurs after the protein is made, which means after transcription and splicing has already happened. +5  
ngman  Also I believe mRNA refers to after the splicing already occurs. If the protein products are from the same mRNA then it can't be alternate splicing. +  
medschul  They're cleaved by tissue-specific proteases +  
duat98  I think: Alternative splicing occurs with hnRNA not mRNA. You get mRNA from alternatively splicing the hnRNA. an mRNA can only make 1 type of protein. Since the question says the 2 proteins comes from the same mRNA it cannot be alternative splice or post transcriptional mod. FA 2018 page 43 has a good illustration. +3  


submitted by seagull(437),

The semantics of this question made me vomit blood.

One day a patient will look me in the eyes and ask, "Where are tripetides broken down?" I will smile at them and say, "the intestinal mucosa and not the duodenum." They'll smile back and I'll walk away and think of this moment as I jump from the window.

sympathetikey  Too real. +2  
mcl  how do i upvote multiple times +6  
trichotillomaniac  I made an account solely so I could upvote this. +4  
dragon3  ty for the chuckle +1  
cinnapie  @trichotillomaniac Same +2  


submitted by mcl(220),

Since you're losing all your bicarb into your pee, you would expect the pH to be more alkaline. Also, since there is decreased Na+/H+ antiport, there is less sodium reabsorbed and therefore increased loss of free fluid to the urine.

mcl  useful figure http://users.atw.hu/blp6/BLP6/HTML/common/M9780323045827-036-f002.jpg +  
joker4eva76  Why wouldn't this be similar to a Type 2 RTA where urinary pH <5.5? +1  
mcl  I can't remember exactly what the question was asking off the top of my head, I think it was asking about relative to normal? But I think you're right in that the alpha intercalated cells (AIC) can still dump H+ into the urine and acidify it to an extent. And, like in RTA2, I don't know that the action of the AIC would be able to overcome the bicarb and acidify the urine enough for it to be the usual pH, so the urine should still be more alkaline compared to baseline. Kinda sucks, pH less than 5.5 should technically be acidic but it's alkaline for pee. +  
mcl  JK, normal urine pH is around 4-8, but I guess they consider closer to 5.5 on the more alkaline side...? I guess I would go more off that the alpha intercalated cells can't completely compensate for the amount of bicarb in the pee due to the CA inhibitor, not so much the actual pH. +  
meningitis  Anhydrase inhibitors also affect the anhydrase inhibitors that are used in the AIC in order to excrete the H+. Here is a link:**http://pedclerk.bsd.uchicago.edu/sites/pedclerk.uchicago.edu/files/uploads/distal_0.png** +3  
mcl  ohhhhhhhhhhhhhhhhhhhhhhh my god duh yes thank you <3 +1  
meningitis  Lol yw!! +  


submitted by chris07(14),

Bed bugs themselves are not known to be carriers of illness, but they can leave itchy bites. The girl is likely to scratch these bites, abrade the skin, and thus increase the risk of a staph skin infection (since staph aureus is the most common skin infection pathogen)

mcl  Oh! The article I found said that MRSA has been shown to colonize the saliva of bed bugs for up to like 15 days, and that they isolated MRSA from several specimens. Is it just more likely that the patient scratches it in since staph is e v e r y w h e r e ? +1  
chris07  I mean it’s possible. The last review course I took said that it wasn’t associated with anything. It may be, but either way...same answer :) +1  


submitted by mcl(220),

To expand on this, pathologyoutlines describes the histology of kapowsi sarcoma as "spindle cells forming slits with extravasated red blood cells"

mcl  lul i don't know why i spell kaposi like that, my b +1  
bubbles  This site is super helpful. Thanks for sharing :) +  
mcl  yesssssss ofc <3 I love path outlines +  
usmleuser007  Just realize that spindle cells are similar to the endothelial cells of blood vessels. Anything that have vessel association might have spindle-shaped cells. a. NF-1 b. NF-2 ~ Schwannoma (Antoni A) = Cutaneous neurofibroma ~ high cellularity (w/ palisading patterns with interspersing nuclear-free zones called Verocay bodies c. Leiomyoma (uterus & esophagus) d. Mesothelioma (cytokeratin positive) e. Anaplastic Thyroid cancer (biphasic & along with giant cells) f. Medullary Thyroid cancer (can also have polygonal cells) g. Primary cardiac angiosarcoma (malignant vascular spindle cells) h. Osteosarcoma (bone cancer) (pleomorphic cells) i. Meningioma j. Kaposi's Sarcoma (HHV-8) = Slit-like vascular spaces with plump spindle-shaped stromal cells +1  


submitted by mcl(220),

To expand on this, what we think happens with Parkinson's disease (and parkinsonianism) is an imbalance between dopamine and acetylcholine. It makes more sense if you look at this diagram, paying particular attention to the indirect pathway. Loss of dopaminergic (DA) neurons from the substantia nigra (SNc) results in constant activation of those ACh secreting neurons, which ultimately results in inhibition of thalamus from initiating movements. Therefore, using anticholinergics help with parkinsonianism secondary to haldol.

mcl  Also, you don't wanna use sinemet since that would be counterproductive +  


We're viewing this slice of the spinal cord from the bottom right? The left right labels always mix me up.

mcl  Yeah, I just stared at this again for a solid 5 minutes straight up dying. I think if we're going with the L/R labels as they are shown on the image, imagine the patient lying on their stomach with their feet pointed towards you and it should make sense. +2  


submitted by lfsuarez(65),

When patients are given Nicotinic acid(Niacin) they are told to expect common side effects to occur such as warmth and redness. One can avoid these side effects by taking aspirin

mcl  To expand on this, the flushing/warmth/redness is due to release of PGD2 and PGE2 which is why taking an NSAID helps. +4  


submitted by mcl(220),

Patient most likely has Tay-Sachs disease. This figure nicely shows the biochemical pathway. Recall that both Tay-Sachs and Neimann Pick disease present with a cherry red spot on fundoscopy, but Tay Sachs lacks the hepatosplenomegaly seen in NP.

hungrybox  Man this is such a nice figure except it doesn't have Krabbe disease :( +  
mcl  Here's another one with Krabbe! :) https://epomedicine.com/wp-content/uploads/2017/01/lysosomal-storage-diseases-enzyme-defects.jpg +4  
hungrybox  thank u +  
kjfhewiufh  [special] +  


submitted by seagull(437),

! I hate these with a burning F***ing passion. Thumbs up if you agree

mcl  Amen brother +  
praderwilli  Every morning: "I think i'll go over glycogen storage diseases, lysosomal storage diseases, and dyslipidemias after questions this afternoon." Every afternoon: Nah +8  
mcl  oh my god are you me +  
praderwilli  I recently found a program called Pixorize. It's pretty much Sketchy for biochem. Wish I discovered it sooner cuz it has helped for a lot of the painful things like this! +3  
tentorium  [special] +  
tentorium  [special] +1  
tentorium  [special] +  
drhello  hello +  
burak  Cherry red spot basically means niemann-pick or tay sachs. Two differences between is: 1- No HSM in Tay Sachs, HSM in niemann-pick. 2- Both of them has muscle weakness but there is hyperreflexia in Tay Sachs, but areflexia in niemann pick disease. In stem cell HSM is not described and hyperreflexia noted. +  


submitted by mcl(220),

Since you're losing all your bicarb into your pee, you would expect the pH to be more alkaline. Also, since there is decreased Na+/H+ antiport, there is less sodium reabsorbed and therefore increased loss of free fluid to the urine.

mcl  useful figure http://users.atw.hu/blp6/BLP6/HTML/common/M9780323045827-036-f002.jpg +  
joker4eva76  Why wouldn't this be similar to a Type 2 RTA where urinary pH <5.5? +1  
mcl  I can't remember exactly what the question was asking off the top of my head, I think it was asking about relative to normal? But I think you're right in that the alpha intercalated cells (AIC) can still dump H+ into the urine and acidify it to an extent. And, like in RTA2, I don't know that the action of the AIC would be able to overcome the bicarb and acidify the urine enough for it to be the usual pH, so the urine should still be more alkaline compared to baseline. Kinda sucks, pH less than 5.5 should technically be acidic but it's alkaline for pee. +  
mcl  JK, normal urine pH is around 4-8, but I guess they consider closer to 5.5 on the more alkaline side...? I guess I would go more off that the alpha intercalated cells can't completely compensate for the amount of bicarb in the pee due to the CA inhibitor, not so much the actual pH. +  
meningitis  Anhydrase inhibitors also affect the anhydrase inhibitors that are used in the AIC in order to excrete the H+. Here is a link:**http://pedclerk.bsd.uchicago.edu/sites/pedclerk.uchicago.edu/files/uploads/distal_0.png** +3  
mcl  ohhhhhhhhhhhhhhhhhhhhhhh my god duh yes thank you <3 +1  
meningitis  Lol yw!! +  


submitted by mcl(220),

Pronator teres and quadratus are both supplied by median nerve (C5/C6/C7/C8/T1, so that's not super helpful.) Extension of the forearm is radial nerve (also C5-T1, also not helpful). This does tell us is it can't be isolated median or radial. Triceps tendon reflex is C7/C8, which narrows it down to these two.

Can anyone explain why it's C7 over C8?

joha961  Same question. How could you determine between the specific nerve roots (C7 vs. C8)? +  
mcl  Someone I was talking to (and post below) was saying that first aid mentions triceps is C7, so that's what should've been the big thing for us. +  


submitted by mcl(220),

Since you're losing all your bicarb into your pee, you would expect the pH to be more alkaline. Also, since there is decreased Na+/H+ antiport, there is less sodium reabsorbed and therefore increased loss of free fluid to the urine.

mcl  useful figure http://users.atw.hu/blp6/BLP6/HTML/common/M9780323045827-036-f002.jpg +  
joker4eva76  Why wouldn't this be similar to a Type 2 RTA where urinary pH <5.5? +1  
mcl  I can't remember exactly what the question was asking off the top of my head, I think it was asking about relative to normal? But I think you're right in that the alpha intercalated cells (AIC) can still dump H+ into the urine and acidify it to an extent. And, like in RTA2, I don't know that the action of the AIC would be able to overcome the bicarb and acidify the urine enough for it to be the usual pH, so the urine should still be more alkaline compared to baseline. Kinda sucks, pH less than 5.5 should technically be acidic but it's alkaline for pee. +  
mcl  JK, normal urine pH is around 4-8, but I guess they consider closer to 5.5 on the more alkaline side...? I guess I would go more off that the alpha intercalated cells can't completely compensate for the amount of bicarb in the pee due to the CA inhibitor, not so much the actual pH. +  
meningitis  Anhydrase inhibitors also affect the anhydrase inhibitors that are used in the AIC in order to excrete the H+. Here is a link:**http://pedclerk.bsd.uchicago.edu/sites/pedclerk.uchicago.edu/files/uploads/distal_0.png** +3  
mcl  ohhhhhhhhhhhhhhhhhhhhhhh my god duh yes thank you <3 +1  
meningitis  Lol yw!! +  


submitted by magrufnis(0),

I’m confused about this one. Weakness of extension and pronation of the right forearm, with a decreased triceps muscle stretch reflex. The answer was C7 nerve root, but how are you able to localize to C7 and not C6 or C8? I figured that extension is radial, C5-T1, and pronation is median, also C5-T1. Triceps reflex is C7-C8 (FA2019 says C6-C7). How would you narrow down to just C7 damage?

txallymcbeal  My FA2018 has “C7” bolded, meaning it is the main nerve root. But I also got this one wrong so I can’t be much help besides that. +  
mnemonia  Honestly just a guess but I have this vague understanding that intrinsic hand muscles are C8-T1 so we might’ve expected more hand motor findings as well with a C8 lesion. +1  
theecohummer  I narrowed it down to C7 using the fact that the C7 myotome is elbow extension. I also learned that the C7 nerve root was the main contributor to the triceps DTR so I just went with that. +  
mchu21  They also mentioned that the person had weakness pronating the right forearm which is performed by the biceps. Biceps is innervated by the musculocutaneous nerve which is C5-C7 and that's what helped me pick C7 > C8. +  
mcl  Sorry, I thought the biceps was a supinator of the forearm? +1  
henoch280  yes.. its the supinator not pronator +  


submitted by mcl(220),

Scabies likes to burrow in the areas between the fingers and toes (FA 2019 161) and causes itching. Could also potentially be lice (groin involvement), but treatment for either overlaps -- gotta use permethrin.

kchakhabar  If only one person is there to see the doctor, why would the doctor prescribe medicine even for his family members who are not there? +  
mcl  Unfortunately, both of these are pretty contagious conditions. FA mentions that scabies spreads via skin to skin contact, and goes on to mention that you're supposed to treat close contacts. I think in this scenario it's ok to give permethrin to the family members who are not present but affected (it's also non-prescription in some cases, I believe.) Slightly related note, similar to why you would treat the sexual partner of someone with chlamydia/gonorrhea, or close contacts of someone with n. meningitides infection. +3  


submitted by hayayah(416),

Growth hormone releasing hormone acts via G-coupled receptors. G coupled receptors need GTP to become activated and GTPase to become inactivated.

No GTP-ase --> chronically active growth hormone releasing hormone receptor --> constant activation of adenylyl cyclase / cAMP pathway and release of growth hormone.

mcl  This figure is useful https://ai2-s2-public.s3.amazonaws.com/figures/2017-08-08/a025a0e224d366e987bc15edd0f7764ef5611e0d/4-Figure3-1.png +  
mcl  [link](https://ai2-s2-public.s3.amazonaws.com/figures/2017-08-08/a025a0e224d366e987bc15edd0f7764ef5611e0d/4-Figure3-1.png) +  
meningitis  How did you knkow it was GHRH and not GH perse? +3  
meningitis  nevermind; I just read down below. Thank you +1  


submitted by hayayah(416),

Growth hormone releasing hormone acts via G-coupled receptors. G coupled receptors need GTP to become activated and GTPase to become inactivated.

No GTP-ase --> chronically active growth hormone releasing hormone receptor --> constant activation of adenylyl cyclase / cAMP pathway and release of growth hormone.

mcl  This figure is useful https://ai2-s2-public.s3.amazonaws.com/figures/2017-08-08/a025a0e224d366e987bc15edd0f7764ef5611e0d/4-Figure3-1.png +  
mcl  [link](https://ai2-s2-public.s3.amazonaws.com/figures/2017-08-08/a025a0e224d366e987bc15edd0f7764ef5611e0d/4-Figure3-1.png) +  
meningitis  How did you knkow it was GHRH and not GH perse? +3  
meningitis  nevermind; I just read down below. Thank you +1  


submitted by mcl(220),

Homegirl got some cervical outlet syndrome and should probably take some stuff out of her backpack or get one of those lil roller ones.

mcl  Whoops, my bad, THORACIC outlet syndrome +1  
dr.xx  Stretching, occupational and physical therapy are common non-invasive approaches used in the treatment of TOS. The cervical rib can be surgically removed. +  


submitted by mcl(220),

To expand on this, pathologyoutlines describes the histology of kapowsi sarcoma as "spindle cells forming slits with extravasated red blood cells"

mcl  lul i don't know why i spell kaposi like that, my b +1  
bubbles  This site is super helpful. Thanks for sharing :) +  
mcl  yesssssss ofc <3 I love path outlines +  
usmleuser007  Just realize that spindle cells are similar to the endothelial cells of blood vessels. Anything that have vessel association might have spindle-shaped cells. a. NF-1 b. NF-2 ~ Schwannoma (Antoni A) = Cutaneous neurofibroma ~ high cellularity (w/ palisading patterns with interspersing nuclear-free zones called Verocay bodies c. Leiomyoma (uterus & esophagus) d. Mesothelioma (cytokeratin positive) e. Anaplastic Thyroid cancer (biphasic & along with giant cells) f. Medullary Thyroid cancer (can also have polygonal cells) g. Primary cardiac angiosarcoma (malignant vascular spindle cells) h. Osteosarcoma (bone cancer) (pleomorphic cells) i. Meningioma j. Kaposi's Sarcoma (HHV-8) = Slit-like vascular spaces with plump spindle-shaped stromal cells +1  


submitted by mcl(220),

Since you're losing all your bicarb into your pee, you would expect the pH to be more alkaline. Also, since there is decreased Na+/H+ antiport, there is less sodium reabsorbed and therefore increased loss of free fluid to the urine.

mcl  useful figure http://users.atw.hu/blp6/BLP6/HTML/common/M9780323045827-036-f002.jpg +  
joker4eva76  Why wouldn't this be similar to a Type 2 RTA where urinary pH <5.5? +1  
mcl  I can't remember exactly what the question was asking off the top of my head, I think it was asking about relative to normal? But I think you're right in that the alpha intercalated cells (AIC) can still dump H+ into the urine and acidify it to an extent. And, like in RTA2, I don't know that the action of the AIC would be able to overcome the bicarb and acidify the urine enough for it to be the usual pH, so the urine should still be more alkaline compared to baseline. Kinda sucks, pH less than 5.5 should technically be acidic but it's alkaline for pee. +  
mcl  JK, normal urine pH is around 4-8, but I guess they consider closer to 5.5 on the more alkaline side...? I guess I would go more off that the alpha intercalated cells can't completely compensate for the amount of bicarb in the pee due to the CA inhibitor, not so much the actual pH. +  
meningitis  Anhydrase inhibitors also affect the anhydrase inhibitors that are used in the AIC in order to excrete the H+. Here is a link:**http://pedclerk.bsd.uchicago.edu/sites/pedclerk.uchicago.edu/files/uploads/distal_0.png** +3  
mcl  ohhhhhhhhhhhhhhhhhhhhhhh my god duh yes thank you <3 +1  
meningitis  Lol yw!! +  


submitted by mcl(220),

Deltoid is innervated by axillary nerve, which comes from roots C5/C6. Actions of the deltoid include abduction of the upper extremity.

seagull  I hope everyone memorized every single part of the brachial plexus and all the roots of each, No detail let untouched!!! +5  
mcl  In case anyone else has purged the whole brachial plexus from your memory (like me), this is a great resource linked by another user. https://geekymedics.com/nerve-supply-to-the-upper-limb/ +1  


submitted by seagull(437),

! I hate these with a burning F***ing passion. Thumbs up if you agree

mcl  Amen brother +  
praderwilli  Every morning: "I think i'll go over glycogen storage diseases, lysosomal storage diseases, and dyslipidemias after questions this afternoon." Every afternoon: Nah +8  
mcl  oh my god are you me +  
praderwilli  I recently found a program called Pixorize. It's pretty much Sketchy for biochem. Wish I discovered it sooner cuz it has helped for a lot of the painful things like this! +3  
tentorium  [special] +  
tentorium  [special] +1  
tentorium  [special] +  
drhello  hello +  
burak  Cherry red spot basically means niemann-pick or tay sachs. Two differences between is: 1- No HSM in Tay Sachs, HSM in niemann-pick. 2- Both of them has muscle weakness but there is hyperreflexia in Tay Sachs, but areflexia in niemann pick disease. In stem cell HSM is not described and hyperreflexia noted. +  


submitted by hayayah(416),

lower quadrantanopia: parietal lesion

vs upper quadrantanopia = temporal lesion

mcl  also, to differentiate whether it is the left or right parietal lobe, recall that stimuli from the left visual field hits the nasal side of the left retina and the temporal side of the right retina, then goes to the right side of the brain. [This figure](https://operativeneurosurgery.com/lib/exe/fetch.php?w=600&tok=856a37&media=optictract.jpg) is helpful. +1  
d_holles  So you're saying that there's two crosses, making it ipsilateral? @mci +  


submitted by hayayah(416),

Hyperacute transplant rejection occurs within minutes d/t pre-existing recipient antibodies that react to donor antigen (type II hypersensitivity reaction), activate complement.

mcl  [Useful figures illustrating transplant rejection](https://www.stomponstep1.com/transplant-rejection-hyperacute-acute-chronic-graft-versus-host/) +  


submitted by haliburton(85),

Small cell lung cancer causes SIADH. Location + exclusionary clues.

mcl  To expand, SIADH may also result in euvolemic hyponatremia. This is because, as we know, ADH increases absorption of water and therefore initially results in an increased circulating volume. However, this results in increased stretch of the atria and subsequent secretion of ANP. ANP (atrial natriuretic peptide) then results in loss of sodium and water. +2