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Comments ...

 +0  (nbme24#24)

Lice are small insects that live on the skin. They are often connected to hair on the scalp or in the pubic area. When you have lice, it is called pediculosis.

Scabies is a condition caused by mites, which are tiny, insect-like animals that dig under the skin.

-AAFP https://www.aafp.org/afp/2012/0915/p535-s1.html


 +0  (nbme24#31)

So if a long polypeptide string is generated from signle mRNA then cleaved → post-translational modification.

If modification happens at level of RNA which is cleaved into smaller mRNA that then give proteins → alternative splicing / post-tranSCRIPTIONAL modification.





Subcomments ...

submitted by happysingh(45),
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o,s the yeK owdrs thta no one is neimontign : minctngcmuaoi herlcuhodspya

het tspaopyhh oseg like htsi :

na ainyatolmrmf tgeitns .(.,ei ansdrhbuoaic h)ogreemarh ilyed fiiobrss / iracsrng of eth aocrahnid luiogantrnas t&=g; mrapiide FSC adearnig

teh kye sponti / etpoccns yhte era rtgyin to tset here : 1. od uyo wnok wtah mcaincmngiout yhdroluhseacp otiw(hut emht itlgenl ouy sohet d)wors .2 od uoy nwok 'hwtsa the phgaoyolstypoih (of cgniommintuca hc)updhrelsoay si ?

potentialdoctor1  Exactly. To add to this, communicating hydrocephalus can be subdivided as follows: Normal-pressure hydrocephalus: Chronic/gradual decrease in CSF reabsorption at arachnoid granulations, usually due to calcification due to aging. CSF accumulates slowly, so ventricles are able to widen without causing an important increase in intracranial pressure. Symptoms occur due to compression of periventricular white matter tracts ---> Wacky, wobbly, wet High-pressure hydrocephalus: Acute decrease in CSF reabsorption at arachnoid granulations, usually due to inflammatory state in the subarachnoid space (eg, meningitis, sub-arachnoid hemorrhage). CSF accumulates suddenly, causing an acute-onset increase in intracranial pressure +7  
sunshinesweetheart  not to take away from your perfect explanations, but if it were a woman with neck stiffness and fever (rather than circle of willis rupture) that could lead to increased CSF production, right? I think that's the only case where CSF production would increase. Also I think decr absorption in arachnoid granulations in that situation as well so it'd be a shit question +  
peqmd  If anyone like me also got "decreased absorption in choroid plexus", as their wrong answer it's because the choroid plexus doesn't "absorb" it produces. +9  
alienfever  FA 19 p510 +2  
alienfever  If anyone chose F, communication hydrocephalus is caused by decreased absorption and not increased production. FA 19 p510. +1  
an_improved_me  So she has a leaking aneurysm for how long.. gets it repaired, and then within 2 days has an inflammatory response that leads to decreased CSF absorption at arachnoid granulation... Is it the bleeding associated with the aneurysm causing it? The surgery? I'm inclined to say the latter, given that it happens coincidently after the surgery, and not for however long it was leaking beforehand. Thats what tripping me up. +  


submitted by happysingh(45),
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,so eth Key wdros tath no eon is inignteomn : nonicmtiugcma ryudahlpscheo

eht opshyapth goes ekil sith :

an ymfnmlotarai iegtnst ,(i.e. oahusabndcri ea)ohrgmrhe leydi isfbosri / igrasrcn of eth aranciohd unnlsiroaagt &=gt; apmredii SFC iraeandg

het yke tonisp / ctcnsepo eyth ear tirgyn ot sett eher : .1 od ouy onkw twah cncimagmntuio uharehylpcods iuh(ttwo mhte llginte you ohtse swdor) 2 . do uoy kown a'swht eth otpyhopgislohya (fo ucntaicmginmo )yloperhhuscda si ?

potentialdoctor1  Exactly. To add to this, communicating hydrocephalus can be subdivided as follows: Normal-pressure hydrocephalus: Chronic/gradual decrease in CSF reabsorption at arachnoid granulations, usually due to calcification due to aging. CSF accumulates slowly, so ventricles are able to widen without causing an important increase in intracranial pressure. Symptoms occur due to compression of periventricular white matter tracts ---> Wacky, wobbly, wet High-pressure hydrocephalus: Acute decrease in CSF reabsorption at arachnoid granulations, usually due to inflammatory state in the subarachnoid space (eg, meningitis, sub-arachnoid hemorrhage). CSF accumulates suddenly, causing an acute-onset increase in intracranial pressure +7  
sunshinesweetheart  not to take away from your perfect explanations, but if it were a woman with neck stiffness and fever (rather than circle of willis rupture) that could lead to increased CSF production, right? I think that's the only case where CSF production would increase. Also I think decr absorption in arachnoid granulations in that situation as well so it'd be a shit question +  
peqmd  If anyone like me also got "decreased absorption in choroid plexus", as their wrong answer it's because the choroid plexus doesn't "absorb" it produces. +9  
alienfever  FA 19 p510 +2  
alienfever  If anyone chose F, communication hydrocephalus is caused by decreased absorption and not increased production. FA 19 p510. +1  
an_improved_me  So she has a leaking aneurysm for how long.. gets it repaired, and then within 2 days has an inflammatory response that leads to decreased CSF absorption at arachnoid granulation... Is it the bleeding associated with the aneurysm causing it? The surgery? I'm inclined to say the latter, given that it happens coincidently after the surgery, and not for however long it was leaking beforehand. Thats what tripping me up. +  


submitted by xxabi(259),
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Sttne smrbsoioht sv nso-rte.isse ttnSe shmbiosort is an etuca iousloccn fo a yaorcrno arrtey e,ntst hchiw oeftn tlusers ni uatec yaororcn d.ymroesn Can eb epdrnetve by uadl etatepailltn reatphy or gnduguei-tlr tsn.est soe-eissRtn is the arlgaud ngwiaronr fo eth netts enmlu eud to aiinotnmle operoifarl,tni gtiueslnr ni nnaagli sy.mpmtos

sunshinesweetheart  so just to clarify - it's the "symptom-free for 3 months" that rules out thrombosis? +6  
hpsbwz  It's moreso that at rest there's no changes, but during exercise there is. Like the pathophys of stable angina. +6  
suckitnbme  I think it's more because of the 2-month history of PROGRESSIVE angina sx with exertion. This points to a chronic process rather than an acute event. +  
alienfever  Drug-eluting stents prevent re-stenosis (rather than thrombosis) by releasing sirolimus which by blocking cell proliferation. +2  


submitted by sugaplum(376),
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meainnepypphlrlnoao si an lhapa ngsoiat ahtt eisstamltu rraeltuh ohstom mluesc nncooitat.cr - mfor toe,dtaup ,wvoereh ti also ssay ti si not edremmdonec tmeetnrta yoeamnr

ugalaxy  α1 stimulation (via α1 agonist) constricts the bladder sphincter thereby, preventing sudden bouts of micturition during coughing/sneezing (abdominal stress). +7  
sammyj98  I thought that B3 stimulation stopped urination +5  
adong  @sammyj98 B3 would facilitate bladder relaxation +  
hvancampen  @sammyj98- were you thinking of oxybutynin? (thats what I thought of!) According to FA, its used for urge incontinence not stress. +1  
drzed  Nah he/she's talking about Beta-3 receptors which are Gs coupled. Gs increases cAMP thus it would cause smooth muscle relaxation -> bladder relaxation! +1  
donttrustmyanswers  From Mayo: "There are no approved medications to specifically treat stress incontinence in the United States. The antidepressant duloxetine (Cymbalta) is used for the treatment of stress incontinence in Europe, however." +1  
nreid4  @hvancampen oxybutynin is an M3 muscarinic antagonist, not B3. +  
alienfever  I thought about B3 agonist as well and got this wrong. I think maybe B3 agonist can be used for bladder (URGENCY incontinence) where the main issue is detrusor over reactivity. In STRESS incontinence however the problem has nothing to do with detrusor, so we use α1 agonist to constrict the sphincter. +1