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

 +2  (nbme24#48)

PCA stroke: Visual Agnosia [can see, but not recognize objects] and Hallucinations, Contralateral hemianopia with macular sparing, Alexia without agraphia[if dominant hemispehere involved].


 +0  (nbme24#42)

you need a mutation in 2 alleles to get CF [since it is autosomal recessive]/


 +0  (nbme24#42)

Lamins form a nuclear membrane surrounding DNA. imp for structural support, organizing genome, regulating gene transcription. Defective in Progeria and muscular dystrophy.


 +0  (nbme24#22)

Testicular torsion mostly happens in young boys, rarely in adults. Also the pain started at the flanks, which is not how torsion pain starts.


 +1  (nbme24#43)

Stent Restenosis occurs from scar tissue grows over stent causing “neointimal hyperplasia” and narrowing, ischemia symptoms return Tx: prevent by using drig eluting stents eg. Sirolimus. Thrombosis Post stenosis is Acute, stent serves as nidus for thrombus formation usually 2/2 missing mediation. Tx: prevent by using dual antiplatelet treatment [aspirin+clopidogrel/ticagrelor]. After 1 year, endothelization of stent occurs and there is a lower risk of thrombus, Tx lowered to just aspirin.


 +4  (nbme24#9)

Cyclin A,D,E and for G1 to S transition [made in G1]. Cyclin B is for G2 to M transition[made in G2].


 +0  (nbme24#20)

The Ham test is a test used in the diagnosis of paroxysmal nocturnal hemoglobinuria (PNH). The test involves placing red blood cells in mild acid; a positive result (increased RBC fragility) indicates PNH


 +1  (nbme24#38)

Taking excess Levothyroxine will cause, Incr fT4, Incr fT3, decr TSH, decr Thyroidal iodine uptake. Excess liothyronine intake will cause incr T3, Decr T4, decr rT3, Decr TSH, because T4 gets converted to T3 and rT3 in periphery.


 +0  (nbme24#35)

I legit thought her oversized pupils were the problem. What genius decided to use this photo.


 +0  (nbme23#21)

Gene amplification is an increase in the number of copies of a gene without a proportional increase in other genes. This can result from duplication of a region of DNA that contains a gene through errors in DNA replication and repair machinery as well as through fortuitous capture by selfish genetic elements.


 +0  (nbme23#4)

Dont get confused with club feet. Clubfoot is a birth defect where one or both feet are rotated inward and downward.[1][4] The affected foot and leg may be smaller than the other.[1] In about half of those affected, both feet are involved.[1] Most cases are not associated with other problems.[1] Without treatment, people walk on the sides of their feet, which causes problems with walking.[2] The exact cause is usually unclear.[1] A few cases are associated with distal arthrogryposis or myelomeningocele.[2]


 +0  (nbme23#43)

According to the Nurses' Health Study, the risk of pulmonary adenocarcinoma increases substantially after a long duration of tobacco smoking: smokers with a previous smoking duration of 30–40 years are more than twice as likely to develop lung adenocarcinoma compared to never-smokers (relative risk of approximately 2.4); a duration of more than 40 years increases relative risk to 5.[8]

This cancer usually is seen peripherally in the lungs, as opposed to small cell lung cancer and squamous cell lung cancer, which both tend to be more centrally located,[9][10] although it may also occur as central lesions.[10] For unknown reasons, it often arises in relation to peripheral lung scars. The current theory is that the scar probably occurred secondary to the tumor, rather than causing the tumor.[10] The adenocarcinoma has an increased incidence in smokers, and is the most common type of lung cancer seen in non-smokers and women.[10] The peripheral location of adenocarcinoma in the lungs may be due to the use of filters in cigarettes which prevent the larger particles from entering the lung.[clarification needed][11][12] Deeper inhalation of cigarette smoke results in peripheral lesions that are often the case in adenocarcinomas of the lung. Generally, adenocarcinoma grows more slowly and forms smaller masses than the other subtypes.[10] However, it tends to metastasize at an early stage.[10]


 +2  (nbme22#15)

Procarbazine side effect is leukemia. FA 2018 page 428


 +2  (nbme22#49)

The patient is in hospice care. according to Conrad fischer ethics example, a man with COPD in hospice can be given high dose opiates even though there is a risk of respiratory depression becuase the intent to relieve suffering is the highest priority.


 -1  (nbme22#46)

PLica circularis: muscosal folds that extend from distal duodenum to proximal ileum FA2018 pg 356




sahusema  that video was sick

 +1  (nbme21#15)

Eumelanin also helps the choroid limit uncontrolled reflection within the eye that would potentially result in the perception of confusing image


 +2  (nbme21#9)

https://www.ncbi.nlm.nih.gov/pubmed/25382505

PUVA is used to treat Psoriasis and Vitiligo


 +2  (nbme21#45)

At resting membrane potential the NMDA receptors are blocked by Mg2+. The voltage dependent Mg2+ block is relieved upon depolarization of the post-synpatic membrane . The ligand dependent activation of the NMDA receptor requires co-activation by two ligands, namely glutamate and glycine.


 +6  (nbme21#7)

Toluene, the main component of volatile glues, lacquer thinners and aerosol paints is the chemical responsible for most clinical toxicity. Inhalants cause an initial excitatory response through the release of epinephrine and activation of the dopamine system, followed by central nervous system depression mediated by the use of GABA pathway1 It manifests as a sense of euphoria, excitation, dizziness, disinhibited behaviour and exhilaration similar to alcohol intoxication, thus resulting in psychological dependence. Repeated inhalations by the user to prolong the intoxication will develop in headache, slurred speech, diplopia, gait abnormality, delusions, visual hallucinations and disorientation. Behavioural changes and characteristic odour on breath or clothing are helpful clues to detect cases. Suspected users may also complain of cough, stuffy nose, sneezing, flushing, salivation, nausea, vomiting and photophobia. Other signs and symptoms of inhalant abuse include spots or sores in or around the mouth, injected sclera, nystagmus, irritability or excitability, anxiety and sleep disturbances. Paint or other stains on the face, hands, or clothes are other indicators of abuse. Severe dryness of facial skin and mucus membranes can also be a feature of repeated, prolonged use of volatile substances8 . Bacterial infection of the dry and cracked skin may result in perioral and perinasal pyodermas, sometimes referred to as “huffer’s rash”9


 +3  (nbme21#31)

Pain fibers for Parietal pleura: Cervical and Costal parts is by Intercostal Nerve, Diaphragmatic and Mediastinal via Phrenic Nerve. Rib cage injury causes costal pleural pain.


 +0  (nbme21#15)

The chemotactic factors produced by monocytes and mast cells and the local vasodilatation stimulates neutrophilic chemotaxis. Also, endothelial cells activation further aggravates the inflammatory response and migration of neutrophils. This leads to an influx of neutrophils locally.

refrence: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5512152/

bronchophony  Why not complement activation?

 +1  (nbme21#24)

Fatty Change in Liver [2/2 High NADH made by ADH and AldDH -> inhibits FA oxidation, impaired lipoprotein assembly and secretion-> FA accumulates.]


 +0  (nbme21#32)

Usual interstitial pneumonia (UIP) is a form of lung disease characterized by progressive scarring of both lungs.[1] The scarring (fibrosis) involves the supporting framework (interstitium) of the lung. UIP is thus classified as a form of interstitial lung disease. The term "usual" refers to the fact that UIP is the most common form of interstitial fibrosis. "Pneumonia" indicates "lung abnormality", which includes fibrosis and inflammation. A term previously used for UIP in the British literature is cryptogenic fibrosing alveolitis (CFA), a term that has fallen out of favor since the basic underlying pathology is now thought to be fibrosis, not inflammation. The term usual interstitial pneumonitis (UIP) has also often been used, but again, the -itis part of that name may overemphasize inflammation. Both UIP and CFA have been described as synonymous with idiopathic pulmonary fibrosis.


 +0  (nbme20#37)

A rapid reduction of ascites is often accomplished simply with the addition of low-dose oral diuretics in the outpatient setting. First-line diuretic therapy for cirrhotic ascites is the combined use of spironolactone (Aldactone) and furosemide (Lasix) - Clevland Clinic





Subcomments ...

submitted by sattanki(31),

Can’t help much on the exact reasoning why, but there are a few UWorld questions on this where if a neonate has hypoglycemia, ketosis and hyperammonemia, a organic acid disorder should be suspected (propionic acid or methylmalonic acid). Less suspicious of an RTA cause hypoglycemia is not characteristic of that.

sweetmed  Im assuming because N-acetylglutatmate is an allosteric activator of CPS I needed in urea cycle. and N-AG is made of glutamate and acetyl coA. So in organic acidemias, all the acetyl CoA is being used to make ketones for energy since gluconeogenesis is messed up. So Urea cycle doesnt work as well and NH3 accumulates +1  


submitted by mcl(204),

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. +4  
sweetmed  this helped a lot! +  
roaaaj  Well explained! +  


submitted by nwinkelmann(93),

So, for some reason, neurotransmitters is something I've ALWAYS struggled with... probably because I wasn't taught it well so never really learned it, just learned enough for whatever exam. I just found this boo through NCBI and its FANTASTIC! It's from 2001 so might be old, but it was great. You can search through the book and find the chapters. I pretty much just went through all of the neurotransmitter chapter. https://www.ncbi.nlm.nih.gov/books/NBK10799/

My main take-aways: Glutamate = major excitatory neurotransmitter. Two types of receptors: 1) metabotropic, most of which are presynaptic Gi which leads to decreased NMDA receptor activity and risk of exocitotixicity, or postsynaptic Gq receptors that lead to increase Na+, K+, and decreased glutamate causes depolarization and increased Mg++ displacement and NMDA receptor activity and risk of exocitotxicity, and 2) ionotropic channels including NMDA and AMPA/kainate channels, which all allow nonspecific cation influx, but only NMDA allows Ca++ influx (and only in a voltage dependent manner after sufficient depolarization has displaced the inhibitor Mg++ ion in the channel).

GABA and glycine = inhibitory neurotransmitters. 1) GABA-A and GABA-C = ionotropic channels that lead to eflux of Cl-, and despite this causing depolarization, the neuron still stays below resting potential. GABA-A binding site for barbiturates, steroids, GABA, and picrotoxin = inside pore of channel. GABA-A binding site of benzodiazepines = outside of pore of channel. 2) Glycine channel is a very similar Cl- eflux channel. 3) GABA-B is a metabotropic channel that activates Gi leading to decreased cAMP which activates efflux K+ channels and inhibits Ca++ influx channels leading to hyperpolarization.

Biogenic amines = catecholamines dopamine (coordination of body movement, reward, motivation, reinforcement), norepinephrine (sleep, wakefulness, attention, feeding behavior, epinephrine (lowest concentration in CNS), plus serotonin (sleep, wakefulness, depression, anxiety, nausea) and histamine (arousal, attention, allergy, tissue damage, and may influence blood brain flow). Obviously, all of this is in addition to adrenergic neurotransmission and flight, fright, and fight response.

ATP and other purines = excitatory transmission, co-released with other small-molecule neurotransmitters. Adenosine isn't classically considered a neurotransmitter because it isn't stored/released in Ca++ dependent manner, but derived from ATP before having an excitatory potential.

Acetylcholine = major neurotransmitter involved in neurotransmission via muscarin and nicotinic receptors.

Peptide neurotransmitters = commonly released as propeptide larger precursors that are cleaved by specific enzymes that were in the same neurotransmitter vesicle upon release. Five types = brain/gut peptides, opioid peptides, pituitary peptids, hypothalamic releasing hormones, and those not classified. Examples = precursor that gives rise to substance P (hippocampus, neocortex, and GIT and released from small diameter PNS C fibers that transmit pain and temperature information, powerful hypotensive, inhibited by opioid peptides), neurokinin A, neuropeptide K, and neuropeptide gamma, and opioid peptides including plant alkaloids (like morphine), synthetic opioid derivatives, and endorphins, dynorphins, and enkephalins. In general opioid peptides are depressants (i.e. analgesia mechanism), involved in complex behaviors (sexual attraction, aggressive/submissive behaviors), and implicated (though not definitive) in psychiatric disorders.

Overall, neurotransmitters = type types: small-molecule transmitters and neuropeptides, where small-molecules transmitters are faster and mediate rapid synaptic transmission (i.e. androgen SNS fight/flight/fright quick response), where as neuropeptides (along with biologic amines and some small molecule transmitters) are slower and mediate gradual, prolonged neurotransmission.

Some pictures: http://tmedweb.tulane.edu/pharmwiki/doku.php/overview_of_cns_neurotransmitters, https://www.semanticscholar.org/paper/Targeting-GABAB-receptors-for-anti-abuse-drug-Phillips-Reed/a049643bb25c8631e0267a40182e6d310d1f31fb/figure/0, and https://www.bluelight.org/xf/threads/difference-between-gaba-a-and-gaba-b.733916/#lg=_xfUid-1-1562540128&slide=0

sweetmed  This is amazing. thank you +  
sweetmed  This is amazing. thank you +  


submitted by nwinkelmann(93),

So, for some reason, neurotransmitters is something I've ALWAYS struggled with... probably because I wasn't taught it well so never really learned it, just learned enough for whatever exam. I just found this boo through NCBI and its FANTASTIC! It's from 2001 so might be old, but it was great. You can search through the book and find the chapters. I pretty much just went through all of the neurotransmitter chapter. https://www.ncbi.nlm.nih.gov/books/NBK10799/

My main take-aways: Glutamate = major excitatory neurotransmitter. Two types of receptors: 1) metabotropic, most of which are presynaptic Gi which leads to decreased NMDA receptor activity and risk of exocitotixicity, or postsynaptic Gq receptors that lead to increase Na+, K+, and decreased glutamate causes depolarization and increased Mg++ displacement and NMDA receptor activity and risk of exocitotxicity, and 2) ionotropic channels including NMDA and AMPA/kainate channels, which all allow nonspecific cation influx, but only NMDA allows Ca++ influx (and only in a voltage dependent manner after sufficient depolarization has displaced the inhibitor Mg++ ion in the channel).

GABA and glycine = inhibitory neurotransmitters. 1) GABA-A and GABA-C = ionotropic channels that lead to eflux of Cl-, and despite this causing depolarization, the neuron still stays below resting potential. GABA-A binding site for barbiturates, steroids, GABA, and picrotoxin = inside pore of channel. GABA-A binding site of benzodiazepines = outside of pore of channel. 2) Glycine channel is a very similar Cl- eflux channel. 3) GABA-B is a metabotropic channel that activates Gi leading to decreased cAMP which activates efflux K+ channels and inhibits Ca++ influx channels leading to hyperpolarization.

Biogenic amines = catecholamines dopamine (coordination of body movement, reward, motivation, reinforcement), norepinephrine (sleep, wakefulness, attention, feeding behavior, epinephrine (lowest concentration in CNS), plus serotonin (sleep, wakefulness, depression, anxiety, nausea) and histamine (arousal, attention, allergy, tissue damage, and may influence blood brain flow). Obviously, all of this is in addition to adrenergic neurotransmission and flight, fright, and fight response.

ATP and other purines = excitatory transmission, co-released with other small-molecule neurotransmitters. Adenosine isn't classically considered a neurotransmitter because it isn't stored/released in Ca++ dependent manner, but derived from ATP before having an excitatory potential.

Acetylcholine = major neurotransmitter involved in neurotransmission via muscarin and nicotinic receptors.

Peptide neurotransmitters = commonly released as propeptide larger precursors that are cleaved by specific enzymes that were in the same neurotransmitter vesicle upon release. Five types = brain/gut peptides, opioid peptides, pituitary peptids, hypothalamic releasing hormones, and those not classified. Examples = precursor that gives rise to substance P (hippocampus, neocortex, and GIT and released from small diameter PNS C fibers that transmit pain and temperature information, powerful hypotensive, inhibited by opioid peptides), neurokinin A, neuropeptide K, and neuropeptide gamma, and opioid peptides including plant alkaloids (like morphine), synthetic opioid derivatives, and endorphins, dynorphins, and enkephalins. In general opioid peptides are depressants (i.e. analgesia mechanism), involved in complex behaviors (sexual attraction, aggressive/submissive behaviors), and implicated (though not definitive) in psychiatric disorders.

Overall, neurotransmitters = type types: small-molecule transmitters and neuropeptides, where small-molecules transmitters are faster and mediate rapid synaptic transmission (i.e. androgen SNS fight/flight/fright quick response), where as neuropeptides (along with biologic amines and some small molecule transmitters) are slower and mediate gradual, prolonged neurotransmission.

Some pictures: http://tmedweb.tulane.edu/pharmwiki/doku.php/overview_of_cns_neurotransmitters, https://www.semanticscholar.org/paper/Targeting-GABAB-receptors-for-anti-abuse-drug-Phillips-Reed/a049643bb25c8631e0267a40182e6d310d1f31fb/figure/0, and https://www.bluelight.org/xf/threads/difference-between-gaba-a-and-gaba-b.733916/#lg=_xfUid-1-1562540128&slide=0

sweetmed  This is amazing. thank you +  
sweetmed  This is amazing. thank you +  


Alkylating agents (merchlorethamine) (the other drugs listed are microtubule inhibitors) increase the risk of AML.

keycompany  Additionally, AML is the only answer choice that has multiple blast forms (myeloblasts, promyelocytes, etc.). ALL is characterized by a single blast form (lymphoblasts). +8  
seagull  CML has blasts too but they tend to favor mature forms. +3  
kash1f  You see numerous blast forms == AML, which is characterized by >20% blasts +2  
keycompany  The answer choices are all of lymphoid origin except for AML and Hodgkin Disease. We know Hodgkin Disease is a lymphoma (not leukemia) and would present with lymphadenoapthy. So the answer must be AML #testtakingstrategies +6  
impostersyndromel1000  @atstillisafraud thanks for mentioning the merchlorethamine increasing risk for AML, i was trying to make a connection with the drugs but couldnt. Had to lean on the test taking skills just like key company +  
sweetmed  Procarbazine is alkylating as well. +  


submitted by usmleuser007(113),

This more likely to be diuretics rather than laxatives b/c

the lab study shows a renal dysfunction (BUN & Creatinine are elevated)

Most likely the patient abused loop diuretics; also knows to cause contraction alkaloids, along with renal problems such as interstitial nephritis

endochondral1  would laxatives also have the low potassium? +1  
link981  My question exactly. And what if they were taking Potassium sparing diuretics? Then laxatives would be more likely or am I mistaken? +  
link981  Also creatine is normal, it's at the higher limit of normal so we can't say there is renal dysfunction. The BUN is elevated because patient has metabolic alkalosis with respiratory acidosis. +  
sweetmed  very important to Remember this: Diarrhea causes metabolic acidosis[from bicarb loss in stool], vomiting & loop diuretics cause metabolic alkalosis. +1  
hello  @usmleuser007 not sure your approach is the best way to think about it. The serum Cr is at the upper limit of normal (1.2). And, even if you calculate the ratio of BUN/Cr, it's 21, which would be a PRE-renal issue. +  


submitted by oznefu(7),

I’m having trouble understanding why this is a better choice than Paget disease, especially with the increased ALP?

zelderonmorningstar  Paget’s would also show some sclerosis. +1  
seagull  ALK is increased in bone breakdown too. Prostate loves spreading to the lumbar Spine. It's like crack-cocaine for cancer. +1  
aesalmon  I think the "Worse at night" lends itself more towards mets, and the pt demographics lean towards prostate cancer, which loves to go to the lumbar spine via the Batson plexus. I picked Paget but i think they would have given something more telling if they wanted pagets, histology or another clue +  
fcambridge  @seagull and aesalmon, I think you're a bit off here. Prostate mets would be osteoblastic, not osteolytic as is described in the vignette. +5  
sup  Yeah I chose Paget's too bcz I figured if it wasn't prostate cancer (which as @fcambridge said would present w/ osteoblastic lesions) they would give us another presenting sx of the metastatic cancer (lung, renal, skin) that might point us in that direction. I got distracted by the increased ALP too and fell for Paget :( +  
kernicterusthefrog  @fcambridge, not exactly. Yes, prostate mets tends to be osteoblastic, but about 30% are found to be lytic, per this study: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2768452/ Additionally, the night bone pains point to mets, and Paget's is much more commonly found in the cranial bones and appendicular skeleton, than axial. This could also be RCC mets! +  
sweetmed  I mainly ruled out pagets because they said the physical examination was normal. He would def have other symptoms. +2  
cathartic_medstu  From what I remember from Pathoma: Metastasis to bone is usually osteolytic with exception to prostate, which is osteoblastic. Therefore, stem says NUMEROUS lytic lesions and sounds more like metastasis. +1  


yotsubato  How is that NOT posterior to middle concha? bad question +2  
sympathetikey  @yotsubato - That would have been if it was the spehnoid sinus (I got it wrong too btw) +  
niboonsh  this is a good video if u need a visual https://www.youtube.com/watch?v=mf7rY1VNy70 +1  
sahusema  Sphenoethmoidal RECESS not sphenoethmoidal SINUS +  


with PCT you are supposed to avoid excessive sunlight and UV exposure. Methoxsalen makes your skin more susceptible to UV light.

notadoctor  Wouldn't UV light also be contraindicated in Vitiligo? +2  
sweetmed  Phototherapy with photochemotherapy (PUVA) is a well-known and well-studied modality for the treatment of psoriasis, which involves systemic or topical administration of chemicals known as psoralens and administration of ultraviolet light in increasing dosages after requisite time gap. PUVA is also used in the treatment of widespread vitiligo with moderately good results, though it is being surpassed by ultraviolet B (UVB), which is equally or slightly more efficacious with fewer side effects. +3  
dashou19  Honestly, I didn't even know what Methoxsalen is, just chose the right answer because I know you can not give UV light to people with PCT... +1  


tinidazole preferred due to single dose

sweetmed  or metronidazole +  
niboonsh  what would his diagnosis be tho? +  
lostweightthxnorovirus  @niboonsh Giardia I believe. the trophozoite is pictured in the problem and has a classic "shield-like" appearance. FA 2019 pg. 155 has more information and the sketchy for it was really good! +1  
nwinkelmann  Per FA, DOC for giardia = metronidazole. MOA of metronidazole = formation of toxic free radical metabolites in the bacterial cell wall that damage DNA making it bactericidal and antiprotozoal. Metro treats = GET GAP = giardia, entamoeba, trichomonas, Gardnerella, anaerobes (below diaphragm), and H. pylori (as an alternative to amoxicillin in PCN allergy). Adverse effects = disulfiram-like reaction, HA, and metallic taste. I didn't know what Tinidazole is, and found out it is of the same drug class as Metronidazole, so makes sense why it would also be used for Giardia. For the purpose of the UMSLE 1, though, I think metronidazole would be DOC (especially because tinidazole isn't in FA). +  


submitted by hayayah(399),

By age 75, the thymus is little more than fatty tissue. Fortunately, the thymus produces all of your T cells by the time you reach puberty. They are long-lived and that's why you can lose your thymus without impairment of your immune system.

sweetmed  Memory T cells live for six months or less in healthy humans (Westera et al., 2013), whereas naive T cells can live for up to nine years +1  
whossayin  so the bone marrow does not take the role of the thymus? +  
dr_jan_itor  @sweetmed, does that mean that if someone loses their thymus, they would develop imunodeficiencies appx 9 years later as the naive T cells have died off? +2  
hpsbwz  @dr_jan_itor no, because once all of the thymocytes become T-lymphocytes, they are stored in lymphoid organs until they're needed. this is why removal of the thymus in MG does not cause any immune system deficiency. +1