share email twitter ⋅ join discord whatsapp(2ck)
Free 120  NBME 24  NBME 23  NBME 22  NBME 21  NBME 20  NBME 19  NBME 18  NBME 17  NBME 16  NBME 15  NBME 13 
introducing : the “predict me” score predictor NEW!
Welcome to b1ackcoffee’s page.
Contributor score: 44


Comments ...

 +2  (nbme18#10)

Cohort vs RCT

In cohort study, you don't assign the exposure, you just simply follow them (risk factors).

In RCT, "you assign the exposure" (drug, surgery)


 +1  (nbme23#49)

I don't know this is weird grammar or I overthought!

They asked 'whose expression is regulated by which of the following hormones?"

I knew defect is in GPCR - adrenergic receptors, whose transcription is regulated by corticosteriods. So chose hydrocortisone.

What was the defect in thought process?

b1ackcoffee  Oh, I get it now. defect in signal transduction by GPCR, not in GPCR itslef +2

 +5  (nbme22#23)

I thought regarding this question as HLA gene distribution (en block).

Even if we discard everything and just think about the last sentence (question), for any gene, chance of sibling having exact same allele is 25%

suppose there are 4 alleles for a gene in parents, A,a, B, and b (what I mean to say is all 4 are different in both parents).

Now suppose one daughter has aB genotype. To have exact same alleles, other daughter must have

50% chance of a (among a and A from mother) multiplied by 50% chance of B (among b and B from father)

combined probability for any gene would be 25%.

Please, point out any fault in the reasoning.

cjdinurdreamz  i used the same exact reasoning +

 +1  (nbme22#5)

my problem with this, why can't it be similar to Hep B (circular DNA)? virus is new or hypothetical.

andro  Hep B - is " partially " Double stranded and not fully double stranded . Double stranded Circular does not necessarily denote Hep B even though the virus has a reverse transcriptase . I think they wanted you to pay attention to this . And besides the obvious fact that Hepatitis viruses cause inflammation of the Hepar ( liver) and not encephalon ( brain) +

 -3  (free120#13)

Calcium is low while PTH is high. It’s primary hyperparathyroidism (not secondary). Ans is branch of IJV.

b1ackcoffee  I got that it must be some vein, I just didn’t know the tributaries. Oh well, anatomy fucks me again! +
azibird  I believe this would be more likely called a type of pseudohypoparathyroidism. Akin to PTH resistance, the PTH just can't get out to do its thing. Good catch though, I didn't even get what was happening here. +
azibird  From wikipedia: "Each parathyroid vein drains into the superior, middle and inferior thyroid veins. The superior and middle thyroid veins drain into the internal jugular vein, and the inferior thyroid vein drains into the brachiocephalic vein." https://en.wikipedia.org/wiki/Parathyroid_gland +

 +1  (free120#18)

Any good material for this and lymph node drainage in general? Is this common knowledge or low yield stuff?

cbreland  Got it with process of elimination, seems very low yield +

 +2  (free120#31)

confused why this is not autonomic dysfunction or hyponatremia due to sweating and why is this orthostatic hypotension?

mamed  Not sure if this is correct thinking but how I got this right was: 1. She is hypovolemic 2. Likely retaining salt so water follows (ADH or just renal dynamics in general). This is how I ruled our hypokalemia and hyponatremia 3. If she is hyponatremic b/c sweating then why wouldn't she also be hypokalemic? so both have to wrong because both can't be right 4. Volume depletion ==> orthostatic hypotension +1
blah  I thought that orthostatic hypotension was more of a chronic condition, but I fooled myself into believing that. +
cbreland  I completely read over the initial BP measurement and picked the wrong answer (mostly b/c of that). Test in 4 days lets get it! +3

 +0  (free120#19)

I am wondering which parasite is this actually? --

b1ackcoffee  @mdmofongo I know this. But which parasite is this? +
drblu92  The parasite is most likely Trichuris trichiura (human whipworm). Trichuriasis is often asymptomatic and adult forms can reach 2 cm in length (visible with naked eye). A lot more common in tropical areas but there have been cases in the southeastern US (ex: Kentucky). All other GI worms would present with either a fever or a cough. Treat with mebendazole or albendazole. +6
dhkahat  not trichuris....ascaris +

 +0  (free120#40)

from @melchior

From the UW ID 666 explanation, although type II pneumocytes normally differentiate into type I pneumocytes after proliferation, they do not differentiate in idiopathic pulmonary fibrosis due to altered cell signals and altered basement membrane, which is why type II pneumocytes are increased.

explanation by @benwhite_dotcom is incorrect

peridot  The UWorld example is talking about idiopathic pulmonary fibrosis, whereas benwhite_dotcom was talking about chronic inflammatory pneumonitis, which presents with increased type II pneumocytes (as indicated by the correct answer). +
topgunber  either way destruction of basement membrane leads to type II hyperplasia. It may leads to fibrosis because of destruction of the basement membrane (the point of no return for lung parenchyma). Type I pneumoyctes will not rise in number because the destruction in the basement membrane (they are the vast majority of cells covering alveoli) +

 +1  (free120#1)

If you are making fatty acid, you should not burn it simultaneously.


 +5  (nbme22#18)

as @mtfp said, NRTI need to be phosphorylated by HOST CELL thymidine kinase, mutation in viral kinase has no role in NRTI resistance.

Need to put as separate comment as wrong explanation is at top.


 +2  (nbme24#42)

Any good material to prepare for this kind of stuffs?

apurva  Lord Jesus +10
ozmartini  Had to think back to my cell bio class in undergrad +

 +1  (nbme21#14)

exactly how does maternal hashimoto can cause cretinism?

lola915  Hashimito is caused by antibodies against thyroid peroxidase and thyroglobulin. Those antibodies can cross the placenta and affect babies thyroid gland causing congenital hypothyroidism. +1

 +0  (nbme21#4)

wrist extensors (tennis - backhand)--> lateral epicondyl wrist flexors (golf - think near shot - don't know what it's called) - medial epicondyl

b1ackcoffee  fucked formatting. +
misterdoctor69  I think the word you're look for is "putt." But yup this is right. +




Subcomments ...

submitted by merpaperple(21),

In meiosis I, the gametocyte splits from a single cell (XXYY) -> 2 cells (XX + YY). In meiosis II these two cells split again (-> X + X, Y + Y). Hence in order for a father to pass on both an X and a Y chromosome to his son (eg in Klinefelter syndrome, w/ XXY chromosome), a spermatid must contain both an X and a Y chromosome, which means that there was an error in meisosi I. The stage at which meiosis I occurs is the primary spermatocyte.

b1ackcoffee  Brilliant question and explanation! +1  


submitted by taway(31),
unscramble the site ⋅ remove ads ⋅ become a member ($39/month)

siTh soquneti is rehdpas tgrleys,an btu 'sit easltisylen sgikan "awth udowl nehapp fi sthi owsnam' hpiirydhytmoos mecbea olcrnelntduo eovr eht roscue of her ?rnpe"cynga

nrrutceyl rhe HST is dgoo -;-&tg endcrtlol-lloew rLTOdoHpCT YthmiyihsHIoAPyE hgih HTS -;gt-& reh hhysdtiimyopro sumt NOT be lrloctoelwlend- e(du to sidioruntp of het //TRTTH3T4SH/ ocdieennr ixsa)

,So now ttha we ndrdtusena hatt eht toisqenu si gsaink w"tha luwdo ahpenp if her moydphstiorihy saw "conlrutloedn?

sArewn: mcrtienis

I itnkh ahtt tihs tnoeqisu is rapedsh ulyo,rtasioc btu rfa be ti form em ot cieitricz het EUMLS iinelncgs o.d.bra.

yotsubato  I think that this question is phrased atrociously, Just like the rest of the NBME +19  
b1ackcoffee  exactly how does maternal hashimoto can cause cretinism? +  
notyasupreme  @b1ackcoffee, it's not maternal hashimoto, basically you just have to disregard the ENTIRE question stem and the last part of the sentence (if the mom's TSH goes up) means that there's hypothyroidism going on, which causes cretinism. +2  
b1ackcoffee  Thanks you @notyasupreme! +  


submitted by andro(189),

Step 1 Recognizing its Acute Kidney injury
Step 2 : differentiating between Prerenal (hypotensive) azotemia and Ischemic ATN

From the vignette , Patient is "fully volume restored " ( not hypotensive anymore) but yet he still has a low urine output Note: Failure of AKI to correct after patient is once again euvolemic - would suggest either another prerenal cause such as Heart Failure , Nephrotic syndrome etc or an intrinsic cause like Ischemic ATN

ATN Stages : 1. prodrome
2. Low urine output (Oliguric phase )
3. High urine output (Polyuric phase)

A side note from medscape : Ischemic ATN is a continuum of Prerenal Azotemia . Indeed the cause of the two conditions are the same , ischemic ATN resulting when hypoperfusion overwhelms the kidneys autoregulatory defenses leading to cell death

I think of it as a reversible cause vs an Irreversible one .
Failure of Prerenal Azotemia to correct after fluid resuscitation means it has progressed to the point of cell death ; Acute Tubular Necrosis . (These cells will eventually regenerate with time )

b1ackcoffee  Exactly! +  


submitted by b1ackcoffee(44),

I don't know this is weird grammar or I overthought!

They asked 'whose expression is regulated by which of the following hormones?"

I knew defect is in GPCR - adrenergic receptors, whose transcription is regulated by corticosteriods. So chose hydrocortisone.

What was the defect in thought process?

b1ackcoffee  Oh, I get it now. defect in signal transduction by GPCR, not in GPCR itslef +2  


submitted by b1ackcoffee(44),

Calcium is low while PTH is high. It’s primary hyperparathyroidism (not secondary). Ans is branch of IJV.

b1ackcoffee  I got that it must be some vein, I just didn’t know the tributaries. Oh well, anatomy fucks me again! +  
azibird  I believe this would be more likely called a type of pseudohypoparathyroidism. Akin to PTH resistance, the PTH just can't get out to do its thing. Good catch though, I didn't even get what was happening here. +  
azibird  From wikipedia: "Each parathyroid vein drains into the superior, middle and inferior thyroid veins. The superior and middle thyroid veins drain into the internal jugular vein, and the inferior thyroid vein drains into the brachiocephalic vein." https://en.wikipedia.org/wiki/Parathyroid_gland +  


submitted by b1ackcoffee(44),

I am wondering which parasite is this actually? --

b1ackcoffee  @mdmofongo I know this. But which parasite is this? +  
drblu92  The parasite is most likely Trichuris trichiura (human whipworm). Trichuriasis is often asymptomatic and adult forms can reach 2 cm in length (visible with naked eye). A lot more common in tropical areas but there have been cases in the southeastern US (ex: Kentucky). All other GI worms would present with either a fever or a cough. Treat with mebendazole or albendazole. +6  
dhkahat  not trichuris....ascaris +  


submitted by mdmofongo(-1),

Myeloperoxidase is the only one actually involved in making free radicals. Catalase makes H2O2 into water, Superoxide dismutase eliminates oxygen radicals, LDH makes lactate (no role in bacterial killing), and NO synthase, makes NO.

b1ackcoffee  I thought SOD also comes (second) after pathway (making h2o2) to make HO—Cl +  


submitted by doodimoodi(62),
unscramble the site ⋅ remove ads ⋅ become a member ($39/month)

diD on noe noctei thta the Odsd irato on het top tlfe is wgnor? mA I isgisnm i?hgsmetno fI oyu eactlluca i,t tis' 6 ustj liek het pto tgrhi n..o.e.

mjmejora  thats actually really funny +  
yex  Because I said so, applies here... :-/ +1  
doodimoodi  Cant believe we pay $60 for this crap +41  
aisel1787  best comment doodimoodi) +1  
b1ackcoffee  that fucking threw me off on exam. I was like is there an effect modification by "Not drinking milk". the fuck! +1  


submitted by j000(5),

i got this question wrong, but i think what this question is really asking is what happens in a systemic infection: which is fever

in systemic infection, the most obvious sign to look for is a fever, not necessarily shivering, sweating, heat production by brown fat, etc.

and how does fever occur? like someone already mentioned: pyogenes --> macrophages releasing IL1 and TNF which increases COX activity in hypothalamus perivascular cells, increase production of PGE2 in hypothalamus and reset the temperature set point.

i think the whole phrase "complete transection of the spinal cord superior to the level of sympathetic..." is a distraction. it just tells you that development of a fever has nothing to do with it

j000  development of a fever in systemic infection has nothing to do with sympathetic nervous flow, so even it's injured, fever would still occur. I think this question is just asking how does fever occur in inflammation/infection situation. +  
b1ackcoffee  So, how do you explain the actual fever by just changing the thermostat?? Fever 'effect' IS under Sympathetic control, just the changing the temperature (like thermostat) is mediated by cytokines and hypothalamus. +  
j000  oh i see what you mean, well i didn't know that, so thanks for clarifying that. however, based on your explanation, it would still get us to the right answer which is "alteration of thermostatic set point", not the fever effect itself. +  


submitted by mattnatomy(43),
unscramble the site ⋅ remove ads ⋅ become a member ($39/month)

wAnsre = Dreedsaec liio;bd molanr roannclut ecienorst

I ebeivle thwa yhet rwee girnty ot tdniicae ni sthi istuneoq saw gayooclPhslci eSluax itscnfnyuDo kaa( - oracremfenP )yAtxie.n

nI isht ,seca ti snwt'a so cmuh teh ercpafnremo taht ediworr het m,an tbu he aym be so fdcoeus no ihs elahth sesius tos(p te,)rosk ahtt he si eaulbn ot erfpmor ytleqaeadu. Trhorefe,e hsi ralutan oilidb dluwo eb aesederd.c oeHvwer, ebeusca t'si pocygeshcni ma&p; nto l,oopsghicyi he odulsh lstil eavh nmloar teiitmnhg seconir.et

b1ackcoffee  Wouldn't pshychological SD have normal libido and just performance anxiety? +  


unscramble the site ⋅ remove ads ⋅ become a member ($39/month)

hohAlutg hetre ear on cescpiif rsheep soitcdari,n a FSC aplne wtih ymlots utokcesyle ecntiiasd a laivr ntcnieifo sa( llwe sa the oanmrl .c)elosug So uyo acn leru tou TB, crraosssunidiooe nda ralaibect. nBer/dngsikrkiuzi isng aer aretdel ot n,itngieims utb evne fi yuo tdno' konw what hetso re,a eht uniqsteo ayss atth ether si na oiytrbalamn ni eth ERLMTAPO oebl iitmnn(gies = .emsnegn)i iEtaihecnpsl lodwu eb eht sbte wsarn,e lieaycsple ueeabsc erespH plitiaEcshen tafecsf het topamelr lebo.

taediggity  Also look for Kluver-Bucy like symptoms in the stem +1  
mambaforstep  why? +  
b1ackcoffee  I agree with everything but normal glucose. Glucose here is NOT normal. to quote wiki "The glucose level in CSF is proportional to the blood glucose level and corresponds to 60-70% of the concentration in blood. Therefore, normal CSF glucose levels lie between 2.5 and 4.4 mmol/L (45–80 mg/dL)." +  
baja_blast  NBME reference table gives normal CSF glucose to be 40-70 mg/dL. As far as I'm concerned, for the purposes of the exam the reference table is probably a better source than wiki. +4  


submitted by mdrahimi7(-5),

The answer must be protein regulation not structure ! First of all you know that cystic fibrosis can have several mutation 1.severe splicing defect In which cftr protein is normal but less in concentration due to 3 types of mutation 1_ promotor box defect and leading to less transcription 2_ premature stop codon 3- and reading frame mutation All these mutation leading to less synthesis of normal cftr protein.The second type of mutation is 3 bade deletion that ctfr protein problem is in folding 3. The mutation is in those part of protein which regulates its function like nucleotide binding domain and regulatory domain Actually to clear more this protein has three part Regulatory domain, Nucleotide bonding domain and transmembrane part . And type 4 mutation is that transmembrane part of protein is defective channel will be made but work less. Now as you can see in the first picture that i sent you actually in(( bronchial and respiratory part)) the cftr protein is present that it normally you know that it secrets cl and inhibits na channel on membrane until na +chlorine absorb the h2o to soften the mucus so it means normally in respiratory system this protein secrets cl and regulate the function of na channel. Now according the respiratory problem that the patient had it points to this point that the mutation of this cftr leads to this that this protein can't secret cl +can't regulate the function of na channel so So the type of mutation occurring to this person is with the regualtory part not the structure (cftr protein is present but can't work in this way to secret cl and regulate the na channel. Because you can see that patient mutation of cftr is not so severe (if it was sever I mean the structure of protein has the problem so according this matter that cftr protein are present in different system of our body in respiratory,gis, other salivary gland , liver complication , heart complication , sweat gland all these systoms will be effected ) but the baby just it has problem in respiratory system and sweat gland so it is mild when it is mild so the mutation should be in this way that either structurally cftr is present but less in number or cftr protein is present but the problem is with the regulatory party that just it can't secrete the cl and can't regulate the function of na channel as you can see in this patient respiratory and sweat gland. Finished😊

b1ackcoffee  I thought the same and got it wrong, but answer is conditioning me NOT to overthink and keep it simple. +  


submitted by taway(31),
unscramble the site ⋅ remove ads ⋅ become a member ($39/month)

Tshi toiusqen si dhpaesr erganlt,sy tbu 'tis eestlilsyan aiknsg awth" loudw ppanhe fi isht s'mowan oyihhydrptmios meaebc nlueldocortn rvoe teh resocu fo erh ?aeryn"gpcn

clrytrnue ehr TSH si ogdo &-t-;g wellreotdln-lco dOtoYLymIrPTHiHphECiyA hsTo ghhi HST -;tg-& erh iimsytdhroohyp must NOT eb e-tnlowercoldll (eud to ptidioursn of teh T/H/TRT3T4H/S neoniecdr xsai)

,oS own htta ew ndrtusdaen ttha the unseoitq si gisnka hwta" uwodl hpneap if reh ipdysyhoitrhom was "ceolt?nlunodr

:swAren iecinsrmt

I knthi thta tihs nqseuiot is rhpdsae ctoisaluoyr, tbu rfa eb ti fmro me to rctezciii eht ESLUM nginsclie ..oadr.b

yotsubato  I think that this question is phrased atrociously, Just like the rest of the NBME +19  
b1ackcoffee  exactly how does maternal hashimoto can cause cretinism? +  
notyasupreme  @b1ackcoffee, it's not maternal hashimoto, basically you just have to disregard the ENTIRE question stem and the last part of the sentence (if the mom's TSH goes up) means that there's hypothyroidism going on, which causes cretinism. +2  
b1ackcoffee  Thanks you @notyasupreme! +  


submitted by dr.xx(150),
unscramble the site ⋅ remove ads ⋅ become a member ($39/month)

necsasa-rHheHnsobdle oiqpHa:u tEn = .16 + lOCH(g3o / 00(.3 * )P2a);OC os heer, pH = 6gt2 &.;=9 cuteA aosnmeptdcne(u) pryarim yraptoerrsi hisciswa,o idt tcmlobiea ciiasdso

sbryant6  calculator can't do logs yo. +5  
b1ackcoffee  wow, sherlock! +  


submitted by b1ackcoffee(44),

wrist extensors (tennis - backhand)--> lateral epicondyl wrist flexors (golf - think near shot - don't know what it's called) - medial epicondyl

b1ackcoffee  fucked formatting. +  
misterdoctor69  I think the word you're look for is "putt." But yup this is right. +  


submitted by tsp(0),
unscramble the site ⋅ remove ads ⋅ become a member ($39/month)

Is het nwaom ni het strif reiganoent 1)2( nto dtefaefc eecbuas of lcteompien tnrap)e1(c2?nee has ot ahev eth ittar rfo eth iseesad to voleped in the utefru ai.netoegnr

b1ackcoffee  disease developed due to germline mosaicism (mutation in of the oocyte) +  


submitted by divakhan(14),
This is not XLD, its XLR disease (FA 2020 page 59)

Here, the mother is homozygous for the mutation therefore she displays the disease.

We see that,

  1. It skips generations
  2. Males are more severely affected (die in utero)
  3. Females are affected (only when homozygous)

Here we see, that mother can pass defective X chromosome to 50% females & other 50% will be carriers (healthy X chromosome from father, defective from mother) For males, Mother passes defective X chromosome so they die (only 1 X chromosome)

For the males who are living (III 6,11 shown in pedigree), they have been lucky to survive due to mosaicism! ;)

b1ackcoffee  don't you think you are going through too many hoops (assumptions)? male survive due to mosaicism? Better chance is disease started due to germline mosaicism and it IS XLD. btw the disease is incontinentia pigmenti (not necessary to know). your second last para doesn't make sense, read again with fresh mind and perspective. +1  


submitted by h0odtime(47),
  • Normocytic Intrinsic Hemolytic Anemia: Reticulocyte >>2.5%
  • PEP --> Pyruvate (last step of Glycolysis) second ATP producing step
  • Mature RBC require pyruvate kinase without it they depend on the anaerobic generation of ATP
  • With insufficient ATP, all active processes in the cell come to a halt. Sodium potassium ATPase pumps are the first to stop: increase intracellular K+, water leaves cell with Na+. Cell Shrinks & dies. Body is deficient in RBC + destroyed by lack of ATP = Hemolytic Anemia
  • Inheritance: AR
b1ackcoffee  ermm . buddy, stopping NaKATPase causes RISE in intracellular Na, cell SWELLS and dies. +3  


submitted by madojo(176),

Know your STD's baby ;-) (going through every other choice on this question):

  • Bacterial vaginosis caused by gardnerella vaginallis. Se a thin, off white discharge and fishy smell (fish in the garden). There's no inflammation Lab findings: pH greater than 4.5 (just like trichomoniasis), and a positive whiff test with KOH. Stem will say something about malodorous discharge and show the infamous CLUE CELLS if we are lucky. Not the answer for this question obviously because we would not expect vesicles with this bacterial disease.

  • Candidiasis is going to be your thick cottage cheese discharge, with inflammation. normal pH see pseudohyphae. Treat with topical nystatin, or oral fluconazole unless you're pregnant than use Clotrimazole. Again not going to see any vesicles.

  • Chancroid per uworld is associated with Haemophilus ducreyi you will have a Deep purulent painful ulcer with suppurative lymphadenitis. Will be told that patient has painful inguinal nodes, there may be multiple deep ulcers with gray-yellow exudate. You do cry with H. duCRYi This wouldn't be true for what our patient has in this question because we aren't told of any inguinal adenopathy. a link to a chancroid VDA

  • Chlamydia trachomatis causes lymphogranuloma venereum which is small shallow ulcers, painless, but then the large painful coalesced inguinal lymph nodes aka BUBOES. Compared with gonnorhea the discharge is more thinner and watery. Again not the case here as its painful and no mention of any BUBOOESS. The discharge in gonorrhea is more thicker. Both lead to PID, treat for both because confection is common. With both patient may have some sort of pain or burning sensation upon urination. Sterile pyuria though for both.

  • Condyloma accuminatum is a manifestation of HPV 6 + 11 (genital warts). They look like big cauliflowers. This is in contrast to Condyloma lata that you see in syphillis which is just a flatter latte brown looking macule.

  • Genital Herpes (the answer to the question) will present with multiple painful superficial vesicles or ulcerations with constitutional symptoms (fever, malaise) Just fits better than all the other choices I ran through.

  • Syphillis is the painless chancre. UW describes it as a single, indurated well circumscribed ulcer, with a clean base. See corkscrew organisms on DF microscopy. Keep in mind other painless ulcers are lymphogranuloma venereum of clamydia (but the buboes are whats painful not the ulcer), and granuloma inguinale (donovanosis - klebsiella granulomatis) but whats hallmark about this one is that its painless without lymphadenopathy

In short, be safe.

drdoom  this write-up is AWESOME ... but it also made me vomit. +  
b1ackcoffee  This is awesome, writeup, not the stds. +  
lovebug  FA 2019 pg 184. I summed up @madojo's comment! this patient have "multiple, tender vesicles and ulcer". and scant vaginal discharge. A) Bacterial vaginosis -> NO vesicle -> r/o B) Candidiasis -> NO vesicle -> r/o C) Chancroid -> should have Inguinal Adenopathy -> r/o D) C. trachomatis -> have Large painful inguinal LN -> r/o E) Condyloma acuminata -> Big Cauliflower -> r/o F) Gental herpes -> YES!!! G) Gonorrhea -> NO Vesicle, creamy prulent discharge -> r/o H) C. trachomatis again (same as D) -> r/o I) Syphilis -> painless chancre -> r/o J) Trichomoniasis -> strawberry cervix, motile in wet prep -> r/o thanks @madojo! +  


submitted by saqeer(1),

a little misleading her increase in weight made it seem as if she had low thyroid hormone and tyrosine is a precursor.

b1ackcoffee  but hypothyroidism would decrease the height. +  


submitted by usmleuser007(395),
unscramble the site ⋅ remove ads ⋅ become a member ($39/month)
.1 heerT" ALH fsna wlil ytr het"
m    .a irnoeTenh = eTrhe 
    .b snt;iHidie Anirgeni; iLsney = AH
L    c. llnnyaPeaehni = 
sfan    d. eaV;iln lisIou;nece eueniLc = 
liwl    e. noytTraphp = r
ty    f. tniihoneeM = 
htme
pparalpha  Thanks! Good mnemonic +1  
b1ackcoffee  best mnemonic +  


submitted by drzed(219),

Perhaps this is an incorrect way of thinking about this, but I always associate the virulence of Strep pneumo to its capsule, but I only associate the K capsular antigen of E. coli to meningitis (recall that E. coli has other specific virulence factors like fimbriae for UTI).

So basically, I figured that the capsule of Strep pneumo is involved in more disease processes (MOPS) than the capsule of E. coli (mostly meningitis), and thus I chose Strep.

b1ackcoffee  You are right, this is INCORRECT way. Capsule helps in hematogenous spread by protecting from phagocytosis causing sepsis, meningitis, pneumonia, i.e. more systemic infections. +