need help with your account or subscription? click here to email us (or see the contact page)
join telegramNEW! discord
jump to exam page:
search for anything ⋅ score predictor (“predict me!”)

Welcome to md_caffeiner’s page.
Contributor score: 83


Comments ...

 -1  visit this page (nbme18#32)
get full access to all contentbecome a member

yo sketchy veterans.

do you remember that loping back and forth lop eared rabbit that was increasing the phasic segmentation and therefore icreasing stool transit time?

This is it now.

get full access to all contentbecome a member
jaramaiha  back and forth.....back and forth.....:D +1
namesthegame22  MOA of Loperamide +

 +7  visit this page (nbme20#5)
get full access to all contentbecome a member

https://imgur.com/a/lCFnj1e FA19 P489 Cerebral cortex regions

get full access to all contentbecome a member

 +14  visit this page (nbme20#12)
get full access to all contentbecome a member

what to do with the NONADHERIANT BADDIES???

Intention to treat, "i had the intention to treat so i am gonna leave in this group no matter what"

as treated , "he is not treated as it is so im gonna change his group to control"

per protocol, "you are fired from all of it, protocols bitch"

get full access to all contentbecome a member
johnfred4  I'm just gonna make an Anki cloze card directly from this +
makingstrides  UWORLD QID 19406 Exact question +

 -2  visit this page (nbme20#17)
get full access to all contentbecome a member

FA19 P592: Renovascular disease: Renal impairment due to ischemia from renal artery stenosis or microvascular disease.  renal perfusion (one or both kidneys) Ž INC renin Ž INC angiotensin Ž HTN. Main causes of renal artery stenosis: ƒ Atherosclerotic plaques—proximal 1/3rd of renal artery, usually in older males, smokers. ƒ Fibromuscular dysplasia—distal 2/3rd of renal artery or segmental branches, usually young or middle-aged females. Clinically, patients can have refractory HTN with negative family history of HTN, asymmetric renal size, epigastric/flank bruits. Most common cause of 2° HTN in adults. Other large vessels are often involved

FA19 P 596: Angiotensin- converting enzyme inhibitors Captopril, enalapril, lisinopril, ramipril. mEChANism Inhibit ACE Ž DECR AT II Ž DECR GFR by preventing constriction of efferent arterioles. INCR renin due to loss of negative feedback.

get full access to all contentbecome a member

 -4  visit this page (nbme20#3)
get full access to all contentbecome a member

this question is gramatically wrong, just move on. i did not and wasted maybe 5 minutes. just know that when you decrease chol. , there is no chol. left, so LDL regulating people open more receptors to balance the chol. back to its normal.

get full access to all contentbecome a member
md_caffeiner  and if you dont even remember what makes what, just know that when ldl is getting into the cell via ldl r., it is going directly to make some chol. +6

 +2  visit this page (nbme20#33)
get full access to all contentbecome a member

Easy AF explanation for doing mitoch. q's: Mothers have diseased children; Fathers don't

Dont forget this trick.

get full access to all contentbecome a member




Subcomments ...

submitted by famylife(110), visit this page
get full access to all contentbecome a member

"Despite inhibition of HMG-CoA reductase by statins, cells compensate by increasing enzyme expression several fold. However, the total body cholesterol is reduced by 20%–40% due to increased expression of LDL receptors after statin administration."

https://www.sciencedirect.com/topics/biochemistry-genetics-and-molecular-biology/hmg-coa

get full access to all contentbecome a member
md_caffeiner  fuck GoT, knowledge is power +1
dhpainte22  Another bullshit question that should've been straight to the point. Statins increase ldl receptors and inhibit hmg coA reductase. This should be simple but nbme can't live with that :( +5
jurrutia  I think they want to test not just your understanding of how statins work, but also the basic principle that when you block X the body tries to compensate by upregulating X. +9


submitted by spow(50), visit this page
get full access to all contentbecome a member

Here's how I thought through this. problem with DCML (absent proprioception and vibration sense), problem with deep tendon reflexes (DRGs), ataxic gait (spinocerebellar pathway), mild weakness (motor neurons). The only thing that all of these pathways have in common is that they all use myelinated afferents.

I don't know if Guillan Barre would actually present like this, but you don't have to know what the illness is to figure the question out.

get full access to all contentbecome a member
queestapasando  Might be acute inflammatory demyelinating polyradiculopathy (FA 2019 p.512): "Most common subtype of Guillain-Barré syndrome. Autoimmune condition that destroys Schwann cells via inflammation and demyelination of motor fibers, sensory fibers, peripheral nerves..." +5
md_caffeiner  sounds really great, and i thought the same and answered the same way. but while in the exam, i had that "how THE FUCK could motor weakness be an afferent??" moment. quite frequently forget the fact that this is an nbme full of mess. lol. +6
2059nyc  It could be explained by the lack of the sensory component for the DTR and not the motor neurons? +2
sonofarathorn  I focused on the loss of vibration and joint position sensation. Pacinian corpuscles sense vibration. Meissner corpuscles and Merkel discs sense position. These sensory receptors are all large myelinated afferents FA 2019 p.482 +2
mgadda  the question asks the most likely explanation for the SENSORY findings +6
aaftabsethi1  Can anyone explain numbness and tingling ? Isnt that through unmyelinated fibres? +1
cassdawg  @aaftabsethi unmyelinated afferents include fibers that carry: slow pain, heat, and olfactory senses. +


submitted by bingcentipede(359), visit this page
get full access to all contentbecome a member

Good explanation on reddit: https://www.reddit.com/r/step1/comments/d8aqj5/spoiler_nbme_16_hey_can_anybody_advice_how_to_get/

Essentially, A = mucinous glands (foamy cytoplasm) B = parietal cells (stain eosinophilc, P ar I etal cells stain PInk w/ a fried egg appearance. Additionally, they're above chief cells C = chief cells (stain basophilic, super dark, and below parietal cells)

get full access to all contentbecome a member
md_caffeiner  reddit: Its not about histology knowledge, you just need to know two things about parietal cells - they are eosinophilic on histo and they are located more superficially compared to chief cells (super basophilic, labeled as C). If you know chief cells are C, mucinous glands are A due to the foamy cytoplasm, the answer has to be B. +
md_caffeiner  reddit2#You're exactly right (although I would say it is histology knowledge). Gastrin stimulates both parietal and chief cells but only parietal cells release hydrogen ions (and chloride ions - to make HCl). ArtiomK is right about the staining and location of parietal cells being highly acidophilic (pink) and predominantly at the apical part of the gastric gland - they're often described as having a fried egg type of appearance (big, round cytoplasm [egg white] with a central, round [yolk] nucleus). Chief cells produce pepsinogen (enzyme) so display the basal basophilic (purple) staining and they're found predominantly at the base of the gastric gland. So, it's a mix of theory and practical understanding - knowing the structure and function of the gastric gland and then the practical histology of the gland (and its cellular composition). +1
md_caffeiner  dont go to reddit and get distracted for 15 minutes lol +14
deberawr  it's better than redownloading tiktok and getting distracted for 3 hours lol (don't do what i did its embarrassing) +


submitted by bingcentipede(359), visit this page
get full access to all contentbecome a member

Good explanation on reddit: https://www.reddit.com/r/step1/comments/d8aqj5/spoiler_nbme_16_hey_can_anybody_advice_how_to_get/

Essentially, A = mucinous glands (foamy cytoplasm) B = parietal cells (stain eosinophilc, P ar I etal cells stain PInk w/ a fried egg appearance. Additionally, they're above chief cells C = chief cells (stain basophilic, super dark, and below parietal cells)

get full access to all contentbecome a member
md_caffeiner  reddit: Its not about histology knowledge, you just need to know two things about parietal cells - they are eosinophilic on histo and they are located more superficially compared to chief cells (super basophilic, labeled as C). If you know chief cells are C, mucinous glands are A due to the foamy cytoplasm, the answer has to be B. +
md_caffeiner  reddit2#You're exactly right (although I would say it is histology knowledge). Gastrin stimulates both parietal and chief cells but only parietal cells release hydrogen ions (and chloride ions - to make HCl). ArtiomK is right about the staining and location of parietal cells being highly acidophilic (pink) and predominantly at the apical part of the gastric gland - they're often described as having a fried egg type of appearance (big, round cytoplasm [egg white] with a central, round [yolk] nucleus). Chief cells produce pepsinogen (enzyme) so display the basal basophilic (purple) staining and they're found predominantly at the base of the gastric gland. So, it's a mix of theory and practical understanding - knowing the structure and function of the gastric gland and then the practical histology of the gland (and its cellular composition). +1
md_caffeiner  dont go to reddit and get distracted for 15 minutes lol +14
deberawr  it's better than redownloading tiktok and getting distracted for 3 hours lol (don't do what i did its embarrassing) +


submitted by bingcentipede(359), visit this page
get full access to all contentbecome a member

Good explanation on reddit: https://www.reddit.com/r/step1/comments/d8aqj5/spoiler_nbme_16_hey_can_anybody_advice_how_to_get/

Essentially, A = mucinous glands (foamy cytoplasm) B = parietal cells (stain eosinophilc, P ar I etal cells stain PInk w/ a fried egg appearance. Additionally, they're above chief cells C = chief cells (stain basophilic, super dark, and below parietal cells)

get full access to all contentbecome a member
md_caffeiner  reddit: Its not about histology knowledge, you just need to know two things about parietal cells - they are eosinophilic on histo and they are located more superficially compared to chief cells (super basophilic, labeled as C). If you know chief cells are C, mucinous glands are A due to the foamy cytoplasm, the answer has to be B. +
md_caffeiner  reddit2#You're exactly right (although I would say it is histology knowledge). Gastrin stimulates both parietal and chief cells but only parietal cells release hydrogen ions (and chloride ions - to make HCl). ArtiomK is right about the staining and location of parietal cells being highly acidophilic (pink) and predominantly at the apical part of the gastric gland - they're often described as having a fried egg type of appearance (big, round cytoplasm [egg white] with a central, round [yolk] nucleus). Chief cells produce pepsinogen (enzyme) so display the basal basophilic (purple) staining and they're found predominantly at the base of the gastric gland. So, it's a mix of theory and practical understanding - knowing the structure and function of the gastric gland and then the practical histology of the gland (and its cellular composition). +1
md_caffeiner  dont go to reddit and get distracted for 15 minutes lol +14
deberawr  it's better than redownloading tiktok and getting distracted for 3 hours lol (don't do what i did its embarrassing) +


submitted by bingcentipede(359), visit this page
get full access to all contentbecome a member

Phenylephrine is an a1>a2 agonist, given as a nasal decongestant. Thanks Sketchy Pharm

get full access to all contentbecome a member
md_caffeiner  I thought exactly the same,thoe brothers in sketchy, but then thought "spring?Sneezing? This is an asthym q and the answer shoud be b agonist" Too much thinking... +3
nikhilredd  a common mechanism between nasal congestion and migraines are vasodilation and their treatment involves vasoconstriction- here alpha agonist +


submitted by huyhoa1qh(-1), visit this page
get full access to all contentbecome a member

2,3-BPG created in RBCs during glycolysis. The production of 2,3-BPG is increased when oxygen availability is reduced, as occurs in chronic lung disease, HF& chronic exposure to high altitudes. Elevated levels of 2,3-BPG decrease Hb O2 affinity, allowing the release of more O2 in the peripheral tissue

get full access to all contentbecome a member
md_caffeiner  you gad one job +7


submitted by medbitch94(56), visit this page
get full access to all contentbecome a member

Actinic purpura results from extravasation of blood into the dermis. This phenomenon is due to the skin atrophy and the fragility of the blood vessels in elderly individuals, which is exacerbated by chronic sun exposure. Actinic purpura lesions are located on sun-exposed areas, like the arms, face, and neck.

Skin atrophy in dermatoporosis is due to an alteration of collagen, similar to that which is seen in osteoporosis. This pronounced skin atrophy caused by the photo-aging makes the dermal vascular network very sensitive to the slightest trauma or shearing force.

get full access to all contentbecome a member
md_caffeiner  Google actinic purpura, look through 5-10 images, and you get the idea. +12
athenathefirst  How can you rule out answer choice (C) autoimmune disease? +
drbravojose  maybe plt is normal +


submitted by hayayah(1212), visit this page
get full access to all contentbecome a member

GnRH agonists like Leuprolide are effective for patients with breast CA because if given in a continuous fashion, they downregulate the GnRH receptor in the pituitary and ultimately decrease FSH and LH.

get full access to all contentbecome a member
md_caffeiner  Quick question: FA19 691 says Leuprolide ClINICAl USE is Uterine fibroids, endometriosis, precocious puberty, prostate cancer, infertility... I guess all except infetility(pulsatile?) are used as continuous? +1
usmlecrasher  GnRH is synthesized and released in pulsatile fashion , so if you give in pulsatile way you induce GnRH effect , and if given in continuous way it will suppress synthesis, depended the desired effect you want to achieve - infertility induce GnRH with pulsatile , stop synthesis for prostate cancer , testicular cancer , hormone dependent Breast cancer give continuous +1
djeffs1  I thought Gonadotropin was released by the Hypothalamus, not the pituitary gland. am I crazy? +
kevintkim4  ^ Gonadotropins are referring to LH/FSH; Gonadotropin-releasing hormone (GRH) is released by the hypothalamus +2
shakakaka  *GnRH +1
dlakaswnd  ffffff.. the way they worded question was so confusing. +


submitted by xxabi(293), visit this page
get full access to all contentbecome a member

Vinca and plant alkaloids bind B-tubulin, which inhibits the formation or disassembly or microtubules, respectively.

get full access to all contentbecome a member
md_caffeiner  Vinca is a plant alkaloid and it has vinblastin, vincristine, which bind β-tubulin and inhibit its polymerization into microtubules Paclitaxel hyperstabilizes and prevents breakdown, its not a Vinca alkaloid. (FA+Wikipedia) +2
md_caffeiner  What I mean is they are both derived from plants. +


submitted by xxabi(293), visit this page
get full access to all contentbecome a member

Vinca and plant alkaloids bind B-tubulin, which inhibits the formation or disassembly or microtubules, respectively.

get full access to all contentbecome a member
md_caffeiner  Vinca is a plant alkaloid and it has vinblastin, vincristine, which bind β-tubulin and inhibit its polymerization into microtubules Paclitaxel hyperstabilizes and prevents breakdown, its not a Vinca alkaloid. (FA+Wikipedia) +2
md_caffeiner  What I mean is they are both derived from plants. +


submitted by dickass(127), visit this page
get full access to all contentbecome a member

Paclitaxel hyperstabilizes polymerized microtubules (made up of alpha- and beta- tubulin)

get full access to all contentbecome a member
md_caffeiner  And clinical use is in breast and ovarian CA (FA19 433) +2
len49  TAXes stabilize society. +1
alimd  Tarzan: taxanes (e.g. paclitaxel, docetaxel, cabazitaxel. SKETCHY +1


submitted by hayayah(1212), visit this page
get full access to all contentbecome a member

The only time you transfuse a Jehovah's Witness patient is when the patient is a minor (<18 years old).

get full access to all contentbecome a member
medstudent65  I get why the answer is not to proceed but simply stating at admissions you dont want blood products means nothing without proper paperwork being signed. +
md_caffeiner  @medstudent65 From what I recall paperwork is needed for example: if the pt is unconscious and wife says that he is Jehovah's Witness. +


submitted by xxabi(293), visit this page
get full access to all contentbecome a member

Bile salts help dissolve gallstones that have formed in the gallbladder, used in patients refractory to surgery or prefer to avoid it.

get full access to all contentbecome a member
xxabi  To add, bile salts are amphipathic which allows for the emulsification and solubilization of lipids in an aqueous environmen +7
md_caffeiner  To add more for people like me who dont even know what amphipathic means:, am·phi·path·ic /ˌamfəˈpaTHik/ (of a molecule, especially a protein) having both hydrophilic and hydrophobic parts +9


submitted by nwinkelmann(366), visit this page
get full access to all contentbecome a member

This explains it really well with a picture: https://www.med.illinois.edu/m2/pathology/PathAtlasf/Atlas01.html.

Hydropic change = one of the early signs of cellular degeneration in response to injury that results in accumulation of water in the cell. Hypoxia/ischemia leads to decease in aerobic respiration in the mitochondria and decreased ATP production due to failure of the Na+/K+ ATPase leading to Na+ and water diffusion into the cell. Individual tubule cells appear swollen and "empty" with almost occluded lumen, glomerulus is hypercellular.

get full access to all contentbecome a member
dickass  it's basically from pathoma chapter 1: cellular injury causes swelling +7
md_caffeiner  @dickass you why arent you on every q stem? +2
mangotango  do you mean "causing failure of the Na+/K+ ATPase" instead of "due to failure of Na+/K+ ATPase..." ? The low ATP is due to dec aerobic respiration, I believe. +2
fatboyslim  @Mangotango yes exactly. Na/K ATPase stops working due to the lack of ATP. I think nwinkelmann mixed it up +1


submitted by md_caffeiner(83), visit this page
get full access to all contentbecome a member

this question is gramatically wrong, just move on. i did not and wasted maybe 5 minutes. just know that when you decrease chol. , there is no chol. left, so LDL regulating people open more receptors to balance the chol. back to its normal.

get full access to all contentbecome a member
md_caffeiner  and if you dont even remember what makes what, just know that when ldl is getting into the cell via ldl r., it is going directly to make some chol. +6


submitted by rio19111(16), visit this page
get full access to all contentbecome a member

Diagnosis: Pneumomediastinum (FA 2019, 659)

+Hamman Sign=Crepitus on cardiac auscultation

Etiology: spontaneous (due to rupture of pulmonary bleb) or 2° (eg, trauma, iatrogenic, Boerhaave syndrome).

get full access to all contentbecome a member
md_caffeiner  also look on FA 667 traumatic pnx where it says "rib fracture" +1


search for anything NEW!