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Welcome to cassdawgโ€™s page.
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 +0  visit this page (nbme15#28)
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Tetracyclines are bacteriostatic and bind the 30S subunit to prevent attachment of aminoacyl-tRNA. Doxycycline and other tetracyclines are commonly used for refractory acne.

Other answers:

  • Ciprofloxacin is a fluoroquinilone that inhibits DNA gyrase/topoisomerase II
  • Erythromycin is a macrolide that inhibits protein synthesis by blocking translocation (macroslide) binding the 23S of the 50S ribosome subunit
  • Penicillin is a beta lactam that is a D-Ala-D-Ala analog that binds to penicillin binding proteins (transpeptidases) and blocks peptidoglycan cross-linking
  • Rifampin is an antimycobacterial drug which inhibits DNA dependent RNA polymerase
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whk123  If this can help too, mnemonic= I have to serve (30 cups of TeA) either its going to be from tetracycline or aminoglycoside family. Aminog ruled out as it is bactericidal and q.stem mentions bacteriostatic so tetra is the answer. +

 +3  visit this page (nbme15#22)
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Pulsatile mass in the abdomen combined with severe abdominal pain, decreased blood pressure, pail and lethargic all point to dissection of an abdominal aortic aneurysm. This would cause decreased femoral pulses due to loss of blood flow to the lower extremities.

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 +1  visit this page (nbme15#20)
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Clostridium perfringins is a common cause of myonecrosis and would be described as a large gram(+) rod (FA2020p138).

  • Bacillis subtilis is a motile gram + rod known as hay bacillis found in soil and the intestines of humans. It is almost never pathogenic and used in probiotic supplements.
  • Bacteroides fragilis is an anaerobe like clostridia but it is a gram negative rod. It is found in lung abscesses from aspiration.
  • Listeria monocytogenes is a gram positive rod but it is more associated with consumption of unpasturized dairy or deli meats and it causes listeriosis which can present from mild gastroenteritis to meningitis. It can be associated with sepsis but more commonly in the elderly, immunocompromised, or newborns and would not be associated with myonecrosis.
  • StaphyloCOCCUS aureus is a gram positive cocci.
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whk123  Side note (UW): Clostridium septicum (causes spontaneous gas gangrene, non traumatic and is triggered by underlying colonic malignancy) and Vibrio vulnificus (gram -ve curved rod, u get it from raw oysters, increased risk with Fe-loaded patients or liver disease) also causes myonecrosis/ necrotizing fascitis. +1
fatboyslim  ^UW# 15027 +

 +17  visit this page (nbme15#41)
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Here, we want to know loading dose which is equal to the volume of distribution x target concentration in plasma.

So our loading dose = 1.81L/kg x 10mg = 18.1mg/kg

She is a 55kg person so 18.1mg/kg x 55kg = 995.5 mg which approximates to 1000mg total loading dose.

Important Pharm Equations to Remember

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cassdawg  10mg/L * sorry +1
cheesetouch  fa2018 p229 +2

 +11  visit this page (nbme15#50)
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Botulism toxin acts via proteases that cleave SNARE and prevent acetylcholine release at the neuromuscular junction (FA2020 p132). Thus, it does not directly affect the post-synatpric muscle cell. If you add external acetylcholine, you would still have a completely normal response. This eliminates all but two answers.

The end plate potential (EPP) would be affected by botulism toxin because the end plate potential is the change in voltage that occurs at the postsynaptic muscle motor endplate after an action potential in the motor neuron axon triggers release of many acetylcholine vesicles. Normally, an action potential in the motor neuron will cause influx of calcium that leads to fusion of Ach vesicles (requiring SNARE) and exocytosis, releasing large quantities of Ach into the synapse which can then bind and trigger an EPP in the muscle. With botulism, fusion of the Ach vesicles is inhibited so less Ach is released and the EPP is blunted. Notably, the voltage is the same as the mEPP which is the voltage after random occurrence of Ach release (see below).

A miniature end plate potential (mEPP) is the voltage change that occurs when one vesicle of acetylcholine is released. These occur randomly. mEPP would not be affected by botulism toxin because it is the produce of random fusion of a vesicle which could still occur after administration of botulism toxin.

Here is an image reminding the difference between EPP and mEPP.

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fatboyslim  Cassdawg you the real MVP +

 +1  visit this page (nbme15#47)
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Chloroquine does not adequately kill the dormant liver form of malaria (hypnozoite), and thus for infections that have a hypnozoite stage treatment requires addition of primaquine (which does adequately kill hypnozoites) to prevent relapse from release of the infection back into the blood. [FA2020 p157]

Hypnozoites are the dormant form of malaria in the liver (think hypno as in sleeping from hypnosis). Plasmodium vivax and ovale have the hypnozoite stage and thus require the addition of primaquine.

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cheesetouch  FA2018 p157 too :) +

 +4  visit this page (nbme15#38)
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Clostridium tetani and Cornybacterium diphtheriae are part of an inactivated toxoid vaccine with Bordatella pertussis (Tdap and DTap consist of Tetanus toxoid, diptheria toxoid, and acellular pertussis, hence ap)

FA2020 p111

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 -2  visit this page (nbme15#30)
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Lesion of the hippocampus results in anterograde amnesia (FA2020 p511, think 50 First Dates kind of forgetting).

Also, the hippocampus is one of the most vulnerable places to ischemic injury (pyramidal cells of the hippocampus, p512)

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cheesetouch  FA18 p for list of brain vulnerable to ischemia is P 496. Hippocampus, neocortex, cerebellum (purkinje cells), watershed areas. +1
namesthegame22  Hippocampus is particularly vulnerable to hypoxia injury because of its high metabolic demands. This leads to cytotoxic edema, which manifests as neuronal enlargement in the affected region. +

 +12  visit this page (nbme15#18)
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FA2020 p144

An USMLE testable fact about salmonella species is that antibiotic use actually prolongs the excretion of the organism. Fun fact(?) for memorization as there is no clear answer as to why that I could find.

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hiroshimi  Have a card in Zanki saying this using abx with salmonella can cause HUS so may be it's linked? +

 +1  visit this page (nbme15#9)
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The esophagus is a component of the foregut of the gut tube, which is lined with endoderm. Pure esophageal atresia can occur due to failure to recanalize. (FA2020 p359) See here for slide explanation.

Here is another diagram of the esophagus and laryngotracheal tube development showing the lumen lined with endoderm covered in splanchnic mesoderm.

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 +0  visit this page (nbme16#26)
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The girl is having absence seizures (staring into space, 3 second bursts of 3/sec spike-and-wave activity). The first-line treatment for absence seizures is ethosuximide. (FA2020 p544 and 517)

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sexymexican888  MOA: blocks thalamic T-type Ca2+ channels +1

 +2  visit this page (nbme16#41)
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He presents with an anticholinergic toxidrome: hot as a hare, dry as a bone, mad as a hatter (FA2020 p241, the anticholinergic toxidrome is the same as an atropine overdose and jimsonweed actually contains atropine).

The antidote for antichlinergics is phyostigmine, an acetylcholinesterase inhibitor that acts as an indirect cholinergic agonist. (FA2020 p240)

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topgunber  physostigmine because its liposoluble and has central effects as compared to neostigmine +4
cheesetouch  FA18 p 237,236 +1
topgunber  its you isnt it @cheesetouch +

 +5  visit this page (nbme16#33)
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Cimetidine is one of the cytochrome p450 inhibitors which would allow increase of the concentration of diazepam to toxic levels by inhibiting its elimination. (https://en.wikipedia.org/wiki/Diazepam)

SICKFACES.COM when I Am Really drinking Grapefruit Juice (FA2020 p252)

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drdoom  sickfaces.com is down again .. +4
zalzale96  I low key expected a porn site to open when I click that link :p +13
feochromocytoma  Also a reminder that alcohol can be both an inducer AND inhibitor of the P450 - - - Chronic alcohol is an inducer of P450 Acute alcohol is an inhibitor of P450 +3
dentist  Famotidine- also a H2 blocker, but not cyp450 inh +1

 +2  visit this page (nbme16#49)
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Ondansetron is a powerful antiemetic that works by antagonizing serotonin 5HT3 receptors. It is given for postoperative nausea and chemotherapy-induced nausea (FA2020 p400)

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sexymexican888  Alo scopolamine is for motion sickness (sea sick) +
shieldmaiden  Between scopolamine and ondasteron, ondasteron starts providing relief in 30 minutes while scopolamine needs several hours to work +
sexymexican888  @shieldmaiden yeah thats a valid point, but I think the main reason you would use odansetron is because it is specifically for chemotherapy induced nausea while scopolamine is for motion sickness +2

 +3  visit this page (nbme16#39)
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Give mesna with cyclophosphamide to prevent hemorrhagic cystitis (FA2020 p251)

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 +20  visit this page (nbme16#2)
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This is metastatic renal cell carcinoma (FA2020 p605) for the following reasons:

  • Polycythemia - this is the primary clue, as it is associated with ectopic EPO (erythropoitin) secretion in paraneoplastic syndromes (FA2020 p228), which can be caused by pheochromocytoma, renal cell carcinoma, heptocellular carcinoma, hemangioblastoma and leiomyoma. Of these, only liver and kidney would be a choice given and hepatocellular carcinoma is incorrect because he did not have any associated finding of jaundice, hepatomegaly, ascites, or anorexia (FA2020 p392). Plus, the liver does not commonly metastasize to brain whereas kidney does (FA2020 p223)
  • Hypercalcemia - this is likely indicative of PTHrP secretion, and renal cell carcinoma is one of the cancers that can do this. However, this is fairly nonspecific as there are many cancers that can secrete PTHrP.
  • Heamaturia - suggestive of kidney/urinary tract involvement
  • Negative for carcinoembryonic antigen - this is a nonspecific marker mainly for colon and pancreatic cancers (FA2020 p226)
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hungrybox  WOW. Amazing explanation. Great work!! +
nbmeanswersownersucks  Additionally the histo looks like the Clear cell type of RCC. The large white/clear spaces with "chicken-wire" vessels and stroma between them. +11
hecticsurreyguy  Any idea as to how the " positive epithelial membrane antigen" fits into it being renal cell carcinoma? Also to add to the reasons for it being Kidney, the image that they provide is a classic example of renal cell carcinoma cells. Take note of how the cells look to almost be vacuolated or completely clear of any cytosolic material apart from the nucleus. This the classic presentation for renal "clear cell" carcinoma. +

 +12  visit this page (nbme17#37)
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Yellow nodules (cholesterol deposits) on the achilles tendons have a very high association with Type II familial dyslipidemia, or familial hypercholesterolemia. This is caused most often by a defect in the LDL receptor function. (FA2020 p94)

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cassdawg  NOTE: This patient shows a SELECTIVE increase in LDL so it is a defect in the LDL receptor NOT a defect in ApoB100. A defect in ApoB100 would present with increased VLDL as well! +28
ginachipotle  Note that the answer is ABSENT LDL receptors vs. partial reduction b/c LDL >700 (LDL = 980), indicating individual is likely homozygous for the trait. (FA2020 pg. 94) +12
jdc_md  you trick me nbme. veryy veryy tricky +5
kevinsinghkang  Why not E? partial reduction? +
kevinsinghkang  never mind i see it above now. thanks ginachipotle +

 +19  visit this page (nbme17#1)
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DISTRIBUTIVE SHOCK (I.E. SEPTIC OR ANAPHYLAXIS) ARE THE ONLY SHOCKS WITH INCREASED CARDIAC OUTPUT!

FA2020 p310

This man presents with hypothermia (septic shock can present with hyper or hypothermia), tachycardia, and low blood pressure with increased cardiac output, characteristic of septic shock. Further distributive shock is associated with severe decrease in systemic vascular resistance while other forms of shock have increased systemic vascular resistance.

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psychofromthemidwest  Thank you so much for this!!! +
cheesetouch  FA2018 P305 Shock +
pakimd  hypothermic presentation of septic shock is due to cytokine-induced dysregulation of the temperature control in the hypothalamus and is associated with poorer outcomes +1
dwillis17  FA2019 page 307 +
dwillis17  FA2019 page 307 +

 +35  visit this page (nbme17#0)
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I don't like how they are asking this, but I think what they are getting at is that after the stent placement ("subsequent to the stent placement") there will be reperfusion injury to the myocardial tissue which occurs through free radical injury and therefore membrane lipid peroxidation is the best answer (FA2020 p210 mentions membrane lipid peroxidation as a mechansism of free radical damage and lists reperfusion injury after thrombolytic therapy as a type). Elevations in the cardiac enzymes I assume are because of the injury to the cells.

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zalzale96  Created an account just to up vote this answer +5
cheesetouch  1998 journal via google " Myocardial injury after cardiac surgery with cardiopulmonary bypass may be related to free oxygen radical-induced lipid peroxidation" +
peteandplop  "Evidence suggests that reactive oxygen species (ROS) may play important roles in the pathogenesis in myocardial infarction [2]. Following ischemia, ROS are produced during reperfusion phase [3, 4]. ROS are capable of reacting with unsaturated lipids and of initiating the self-perpetuating chain reactions of lipid peroxidation in the membranes" (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2274989/) +1
mittelschmerz  Honestly the wording got me on this one. Great answer +
acerj  Also, you can rule out a few of the options to help justify this. Post MI you expect necrosis, not apoptosis. Remember, apoptosis is suicide, and necrosis is MURDER! Cell swelling is a sign of cellular injury, not cell shrinkage. The heart will undergo coagulative necrosis, not liquefactive necrosis. Also, protease inactivation by cytoplasmic free calcium is kind of nonsensical to me. Free calcium is more likely to cause cell injury via caspases (a form of proteases amongst other things), which is why calcium is usually bound up inside healthy cells. +5
ownersucks  This question presentation is exactly how Sattar said in pathoma Ch2. Raise in cardiac enzyme following reperfusion +
amy  FA2020 305: Reperfusion injury: free radical and increased Ca influx--hypercontraction of myofibrils There is increased cytoplasmic free calcium ions, but it induces hypercontraction, no protease inactivation. +

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The key here is "wound healing". TGF-beta is a vital cytokine in the healing process as well as in attenuation of immune response (FA2020 p216)

FGF, TGF-beta, VEGF, PDGF, EGF (all GROWTH factors ending in GF which promote healing) as well as metalloproteinases (for remodeling) are vital in the wound healing process.

TGF-beta and IL-10 are the two "resolution" cytokines vital in attenuating the immune response. FA2020 p108 has important cytokines.

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 +1  visit this page (nbme17#38)
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In androgen insensitivity syndrome, the testes may descend and push through into the labia majora. Thus the labia majora corresponds to the scrotum. (FA2020 p639)

Here is a diagram of corresponding embryological structures. FA2020 p622 discusses sexual differentiation but doesn't go as in depth with which exact structures correspond.

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dermgirl  Labioscrotal swelling in the presence of DHT produce the scrotum whereas in the presence of estrogen produce labia majora. FA2020 p623. +1
lovebug  FA2019 p609. +

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The basics of this question are what are the major chemotactic factors that attract neutrophils to the site of injury.

These are: IL-8, C5a, LTB4, kallikrein, and platelet activating factor

FA2020 p406 and 215

Important cytokines are on p108

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sarahhjp  p108 of FAA 2020 says IL-8 is the major chemotactic factor for neutrophils +1

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The Congo Red staining showing characteristic birefringence (usually described as apple green) is indicative of amyloid (FA2020 p212). Her findings are characteristic of secondary amyloidosis with serum amyloid A which can cause restrictive cardiomyopathy and nephrotic syndrome and is associated with rheumatoid arthritis.

Amyloid protein composition is misfolded aggregates of beta-pleated sheets.

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cheesetouch  FA 2018 p218 +1

 +2  visit this page (nbme17#0)
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These individuals have a poluymorphism in the breakdown pathway of 6-MP. Like most polymorphisms in drug breakdown pathways, this will lead to buildup of toxic metabolites unless the drug dose is decreased (i.e. the 6-MP will be shunted into the pathway that makes the toxic 6-thioguanine).

6-MP and its prodrug azothioprine inhibit purine synthesis (FA2020 p36 and p440).

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ali_hassan  my pea-sized brain doesn't understand why not give injections of XO. help +2
harbourlights  that's what I put. Because if you decreased their dosage wouldn't also cause a decrease in the final 6-TGN concentration making it less effective? +2
amira89  what is thiopurine methyltransferase (TPMT) and where does it act? +1
specialist_jello  qid 1890 +1

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Alendronate is a bisphosphonate which acts as a pyrophosphate analog and binds hydroxyapatite in bones and inhibits osteoclast activity. (FA2020 p486)

As a general rule, most drugs of osteoporosis inhibit osteoclast activity and bone resorption somehow (the bisphosphonates, calcitonin mimetics [directly bind a receptor on osteoclasts], estrogens/SERMs [inhibit PTH mediated bone resorption and cytokine secretion], Denosumab [mAb which inhibits RANKL which typically activates osteoclasts]). The ONLY FDA approved medication which has the ability to stimulate bone formation is teriparatide.

(FA2020 p462 osteoporosis)

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cheesetouch  Fa2018 p 471 bisphosphonates (alendronate, ibandronate, risedronate, zoledronate) +

 +8  visit this page (nbme17#33)
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This is a Congenital Diaphragmatic Hernia (FA2020p370).

Conginital diaphragmatic hernias are caused by a congenital defect of the pleuroperitoneal membrane which allows contents of the abdominal cavity to herniate upward, and displace the contents of the thorax (hence why our baby has displacement of the mediastinal contents to the right). This also leads to lung malformation and respiratory distress (hence the low apgar scores). Because the stomach is likely herniates upward, a nasogastric tube placed would appear in the left mediastinum (because that is where the stomach is). Further, there is an absence of bowel gas in the abdomen likely because the bowels are herniated into the thorax.

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cheesetouch  FA2018 P364 CDH +1
randi  FA2019 364 Diaphragmatic Hernia +1
kcyanide101  I had chosen lung hypoplasia in this question.... because i felt the hypoplastic lung creates room for the stomach to herniate into the thoracic region +

 +3  visit this page (nbme19#45)
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Water does not require transport proteins or energy for absorption, and transepithelial transport means it must go through the epithelial cells. C is the best match.

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geekymle  i dont know why i missed it. it was a direct answer! +1

 +0  visit this page (nbme19#37)
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This is neonatal physiologic jaundice (FA2020 p393), which is primarily due to immature UDP-gluconuryosyltransferase causing an unconjugated bilirubinemia. The mechanism is decreased conjugation of bilirubin.

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surgerydoctorca_sgu  Also, keep in mind a few other things with physiological jaundice: It occurs after first 24 hours of life and usually is self resolving after 1-2 weeks. Treatment involves phototherapy (non-UV) isomerizes unconjugated bilirubin to water-soluble form. +

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This is G6PD deficiency. (FA2020 p422)

G6PD deficiency causes a hemolytic anemia when individuals are exposed to antimalarials due to the increased oxidative stress. This is due to the deficiency in replenishing NADPH which is necessary to replinish reduced glutathione which aids in quenching free radicals.

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cbay0509  thank you +1

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Propanolol is a nonselective beta blocker:

  • Blockade of beta-1 receptors: beta-1 typically cause an increase in heart rate, so blockade causes decrease in heart rate and contractility. CO = HR x SV so there is an overall decrease in cardiac output
  • Blockade of beta-2 receptors: beta-2 receptors normally cause relaxation of smooth muscle and vasodilation, so blockade causes constriction and therefore increases total peripheral resistance (decreased radius leads to increased resistance)
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waitingonprometric  giving a non-selective beta blocker will cause unopposed alpha effects (i.e. vasoconstriction), this is the opposite of what you want in this patient +




Subcomments ...

submitted by spow(50), visit this page
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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.

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queestapasando  Might be acute inflammatory demyelinating polyradiculopathy (FA 2019 p.512): "Most common subtype of Guillain-Barrรฉ 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 mousie(272), visit this page
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Why no sweating? I mean I get Ecstasy is probably the drug of choice before an all night dance party (lol) but don't understand why there would be cold extremities and no sweating when is FA it says hyperthermia and rhabdo????

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sympathetikey  FA says, "euphoria, disinhibition, hyperactivity, distorted sensory and time perception, bruxism. Lifethreatening effects include hypertension, tachycardia, hyperthermia, hyponatremia, serotonin syndrome." So I think they wanted you to see Sinus Tachy and jump for MDMA. Idk why Ketamine couldn't also potentially be correct though. +13
amorah  I picked ketamine because it said no diaphoresis. But if you need to find a reason, I guess the half life of ketamine might rule it out. Remember from sketchy, ketamine is used for anaesthesia induction, so probably won't keep the HR and BP high for 8 hrs. In fact, its action is ~10-15 mins-ish iv. +13
yotsubato  Because the NBME is full of fuckers. The guy is probably dehydrated so he cant sweat anymore? +22
fulminant_life  you wouldnt see tachycardia with ketamine. It causes cardiovascular depression but honestly i saw " all-night dance party" picked the mdma answer and moved on lol +10
monkd  Ketamine acts as a sympathomimetic but oh well. NBME hasn't caught on to ketamine as a drug of recreation :) +6
usmleuser007  Why not LSD? +1
d_holles  @usmleuser007 LSD doesn't cause HTN and โ†‘ HR. +2
sbryant6  @fulminant_life FALSE. KETAMINE CAUSES CARDIOVASCULAR STIMULATION. +12
dashou19  Take a look at why the patient has pale and cold extremities. "Mechanistic clinical studies indicate that the MDMA-induced elevations in body temperature in humans partially depend on the MDMA-induced release of norepinephrine and involve enhanced metabolic heat generation and cutaneous vasoconstriction, resulting in impaired heat dissipation." https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5008716/ +5
drzed  @sbryant6 you're both saying the same thing. Ketamine has a direct negative inotropic effect on the heart, but it is also a sympathomimetic. You are both correct. +1
paperbackwriter  @drzed Can you please site that? As far as I understand ketamine has a sympathomimetic effect on the CV system --> increased chronotropy and BP. I also don't see how they're saying the same thing. One person said "stimulation" and the other said "depression" +1
nutmeg_liver  People tend to drink a lot of water on MDMA. I just guessed the confusion was a result of hyponatremia (too much free water) but no idea if there's any data saying that people tend to become hyponatremic due to water over-consumption on MDMA lol. +2
cassdawg  "Despite possessing a direct negative cardiac inotropic effect, ketamine causes dose dependent direct stimulation of the CNS that leads to increased sympathetic nervous system outflow. Consequently, ketamine produces cardiovascular effects that resemble sympathetic nervous system stimulation. Ketamine is associated with increases in systemic and pulmonary blood pressures, heart rate, cardiac output, cardiac work, and myocardial oxygen requirements."(https://www.openanesthesia.org/systemic_effects_of_ketamine/) +1
brise  LSD does cause HTN and tachycardia according to uworld! @d_holles +2


submitted by rossiememe(6), visit this page
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DOSE x F = AUC x CL

(F= Bioavailability)

If dose is constant and F is increased for Drug X then AUC would increase.

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melanoma  and the cl? +2
cassdawg  Clearance is independent of bioavailability as it is determined by the rate of elimination (affected by liver and kidney "clearance" of the drug, not the "absorbability" that is essentially bioavailability) +1


submitted by apurva(101), visit this page
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Lol i thought trauma would hit more superficial structure than deep.. haha

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cassdawg  Literally how I answered this question cause I didn't know what dysmetria was. Convinced myself of some version of coup/contrecoup that would injure this part of the brain and got it right for all the wrong reasons. Wish I could do that more often. +1
faus305  @cassdawg I did the same thing, lol. But I like to think that deep down we knew what we were doing. I knew the cerebellum was involved in balance and that this guy who just crashed his motorcycle would probably be having some balance issues. +1


submitted by greentea733(23), visit this page
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Why wouldn't the body down-regulate the conversion of FT4 into FT3? Is that conversion just constitutively activated? Since FT3 is more potent than T4, it would make sense for the body to turn that conversion down...that was my reasoning...obviously not correct, but idk why that wouldn't be the case. Anyone have insight?

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maria_danieli  i thought the same... i remember that T3 conversion is somehow regulated but evidently not in this case +1
sars  Peripheral conversion of free T4 to T3 is done by 5-deiodinase. From what I know, only way to decrease this conversion is via b-blockers, glucocorticoids, propylthiouracil, and potassium iodide (lugols). I believe this was mentioned in the sketchy pharm vid as well. +2
sars  Peripheral conversion of free T4 to T3 is done by 5-deiodinase. From what I know, only way to decrease this conversion is via b-blockers, glucocorticoids, propylthiouracil, and potassium iodide (lugols). I believe this was mentioned in the sketchy pharm vid as well. +1
sars  4th blocking agent isn't lugols, its iodinated radiocontrast dye! Sorry for that mistake. +1
cassdawg  "T3 is derived from peripheral conversion of T4... normal plasma T3 levels are obtained in athyreotic patients treated with sufficient T4 to achieve high-normal plasma (F)T4 levels. Administration of T4 to hypothyroid rats to achieve normal plasma T4 levels results in subnormal plasma T3 levels not only because of the lack of T3 secretion but also because of a decreased T3 production by D1 in peripheral tissues, since this enzyme is under positive control of T3 itself". (https://www.ncbi.nlm.nih.gov/books/NBK285545/) i.e. because he is taking SUPRATHERAPEUTIC T4 his T3 is NORMAL. If he was taking NORMAL T4 then he would have DECREASED T3. Pretty sure the normal T4/decreased T3 thing is in another NBME test or UWorld somewhere. +1
cassdawg  ^Sorry to add, her is suprasupratherapeutic so his T3 is elevated. Essentially in a normal hypothyroid patient they are given supratherapeutic T4 to get normal T3 since T3 is the hormone with the action. Apologies if anything is confusing. +2


submitted by greentea733(23), visit this page
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Why wouldn't the body down-regulate the conversion of FT4 into FT3? Is that conversion just constitutively activated? Since FT3 is more potent than T4, it would make sense for the body to turn that conversion down...that was my reasoning...obviously not correct, but idk why that wouldn't be the case. Anyone have insight?

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maria_danieli  i thought the same... i remember that T3 conversion is somehow regulated but evidently not in this case +1
sars  Peripheral conversion of free T4 to T3 is done by 5-deiodinase. From what I know, only way to decrease this conversion is via b-blockers, glucocorticoids, propylthiouracil, and potassium iodide (lugols). I believe this was mentioned in the sketchy pharm vid as well. +2
sars  Peripheral conversion of free T4 to T3 is done by 5-deiodinase. From what I know, only way to decrease this conversion is via b-blockers, glucocorticoids, propylthiouracil, and potassium iodide (lugols). I believe this was mentioned in the sketchy pharm vid as well. +1
sars  4th blocking agent isn't lugols, its iodinated radiocontrast dye! Sorry for that mistake. +1
cassdawg  "T3 is derived from peripheral conversion of T4... normal plasma T3 levels are obtained in athyreotic patients treated with sufficient T4 to achieve high-normal plasma (F)T4 levels. Administration of T4 to hypothyroid rats to achieve normal plasma T4 levels results in subnormal plasma T3 levels not only because of the lack of T3 secretion but also because of a decreased T3 production by D1 in peripheral tissues, since this enzyme is under positive control of T3 itself". (https://www.ncbi.nlm.nih.gov/books/NBK285545/) i.e. because he is taking SUPRATHERAPEUTIC T4 his T3 is NORMAL. If he was taking NORMAL T4 then he would have DECREASED T3. Pretty sure the normal T4/decreased T3 thing is in another NBME test or UWorld somewhere. +1
cassdawg  ^Sorry to add, her is suprasupratherapeutic so his T3 is elevated. Essentially in a normal hypothyroid patient they are given supratherapeutic T4 to get normal T3 since T3 is the hormone with the action. Apologies if anything is confusing. +2


submitted by nwinkelmann(366), visit this page
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Does anyone have a good explanation for why decreased levels of inhibin is wrong? From my understanding, inhibin and activin work together, in that inhibin binds and blocks activin leading to decreased feedback on hypothalamus and activin increases FSH and GnRH production.. thus, if you decrease inhibin then you would have increased activin which would lead to increased GnRH and FSH, right? I found one article talking about it in regards to puberty, but it seems to be a hypothesis/not confirmed at this point... is that why? But still... how do I rule it out on a test?

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yb_26  I also picked decreased inhibin. may be it was one of the "experimental questions", which are not even counted on the real exam +2
artist90  Inceased FSH will lead to spermatogenesis and spermiogenesis NOT Increase in Testosterone which is causing increased Height of this pt +7
artist90  Inhibin B only has negative feeback on FSH not GnRH. see the diagram on the topic of semineferous tubules in FA. Testosterone has a negative feedback on BOTH LH and GnRH +3
usmile1  Kind of like how nocturnal pulsatile GNRH release occurs during sleep to stimulate growth (FA page327), the same thing happens for puberty. Pg 325 in FA, "pulsatile GnRH leads to puberty and fertility." It doesn't explicitly state during sleep, but pulsatile release of GnRH leading to pulsatile release of LH and FSH will lead to puberty. Puberty starts in the brain, its onset really has nothing to do with decreased inhibin levels which happens in the testes. hope that makes sense! +4
sars  From what I understand, inhibin is only released by granulosa cells when FSH levels are high. This is a boy. Next off, this question is about puberty, which is due to pulsatile GnRH leading to large amounts of LH and FSH, leading to large amounts of dihydrotestosterone (males) and estradiol (females), and eventually secondary characteristics of puberty. The increased pulse of estrogen and testosterone leads to GH release, which is metabolized into IGF-1 in the liver. This leads to long bone growth from what I understand, which is not much. +1
cassdawg  @sars inhibin B is also released by sertoli cells in males and will feedback to inhibit FSH release, its not just a female thing. Also, there is actually an inhibin B pubertal surge in both females and males that corresponds to maturation of the granulosa and sertoli cells, respectively. Hormones are wack. https://pubmed.ncbi.nlm.nih.gov/15319819/ +1
j44n  I think youre just supposed to see that he's starting puberty and know that the nocturnal pulses are involved +1


submitted by poormedstudent(14), visit this page
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I was trying to figure out how are the catecholamines cause the K shift into the cells. I was not seeing the connection at first. normally in old NBMEs and Uworld questions- Insulin is causing K+ to enter the cells. then I remember seeing the sketchy band camp and in the far right of the sketch there is B2 activation = beta 2 tuba or something.. anyway beta 2 is found on pancreatic beta cells, catacholamines activate beta 2 on pancreatic beta cells which will cause insulin to be released. insulin released causes K to be driven inside the cells, causing the hypokalemia

references:

-FA 2019 pg 238 Beta 2 --> increase in insulin release and increase cellular K+ uptake.

-Linda S. Costanzo's physiology text:image showing insulin and beta agonist driving K+ into the cells

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cassdawg  FA2020 p590 lists all the stuff that causes different potassium shifts +2
syoung07  This is correct but a lot going on. Catecholamines directly stimulate Na/K atpase just like insulin does. +3
ih8payingfordis  FA 2019 pg 578 +1


submitted by andro(269), visit this page
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And just incase you were as curious as I am and wanted to know what tautomerism is.... A tautomer is an isomer , and isomers are compounds that have the same number of atoms of the same element but different structural arrangemennts

A NOTE TO SELF : DO NOT PICK THIS ANSWER IN THE EXAM

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cassdawg  ^^Also looked it up... Tautomerization is technically a mechanism of spontaneous DNA damage because tautomerization of a base can cause it to change its pairing property. But yeah I doubt it will ever be an answer on the exam. +1
cassdawg  According to wiki "Ketoโ€“enol and the analogous aminoโ€“imino tautomerism are among the primary causes of spontaneous mutations during DNA replication and repair" +2


submitted by andro(269), visit this page
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And just incase you were as curious as I am and wanted to know what tautomerism is.... A tautomer is an isomer , and isomers are compounds that have the same number of atoms of the same element but different structural arrangemennts

A NOTE TO SELF : DO NOT PICK THIS ANSWER IN THE EXAM

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cassdawg  ^^Also looked it up... Tautomerization is technically a mechanism of spontaneous DNA damage because tautomerization of a base can cause it to change its pairing property. But yeah I doubt it will ever be an answer on the exam. +1
cassdawg  According to wiki "Ketoโ€“enol and the analogous aminoโ€“imino tautomerism are among the primary causes of spontaneous mutations during DNA replication and repair" +2


submitted by cassdawg(1781), visit this page
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"Simple rules of the brainstem" (credit to our anatomy gods at UofL for organizing, also this image is fucking great for visual learners):

  1. There are 4 structures always in the โ€˜midlineโ€˜ beginning with M
    • Motor pathway (or corticospinal tract): damage results in contralateral weakness of the arm and leg
    • Medial Lemniscus: damage results in contralateral loss of vibration and proprioception in the arm and leg
    • Medial longitudinal fasciculus: damage results in ipsilateral inter-nuclear ophthalmoplegia (failure of adduction of the ipsilateral eye towards the nose and nystagmus in the opposite eye as it looks laterally)
    • Motor nucleus and nerve: damage results in ipsilateral loss of the cranial nerve that is affected (III, IV, VI or XII)

  2. There are 4 structures to the โ€˜sideโ€˜ (lateral) beginning with S
    • Spinocerebellar pathway: damage results in ipsilateral ataxia of the arm and leg
    • Spinothalamic pathway: damage results in contralateral alteration of pain and temperature affecting the arm, leg and rarely the trunk
    • Sensory nucleus of CN V: damage results in ipsilateral alteration of pain and temperature on the face in the distribution of CN V (this nucleus is a long vertical structure that extends in the lateral aspect of the pons down into the medulla)
    • Sympathetic pathway: damage results in ipsilateral Hornerโ€™s syndrome, that is partial ptosis and a small pupil (miosis)

  3. The rule of CN 4โ€™s (also found in FA2020 p504)
    • 4 cranial nerves in the medulla (IX-XII)
    • 4 in the pons (V-VIII)
    • 4 above the pons (2 in the midbrain= III, IV, 2 in the cortex= I, II)
    • The 4 motor nuclei that are in the midline are those that divide equally into 12 (except I and II), including III, IV, VI and XII (V, VII, IX and XII are in the lateral brainstem)
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cassdawg  Sorry for the formatting fuck up +1
drdoom  @cassdawg best to avoid doing nested lists. website doesn't seem to like that :P better to start a โ€œbrand newโ€ list for each little subsection kinda thing :) p.s. congrats on your MVP of the Year Award! +2
unknown001  this is the most complex picture i have seen on brain stem +


submitted by andro(269), visit this page
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As both may occur after trauma Just recall : *Synovial Cyst (ganglion cyst ) - forms a fluctuant mass

*Myositis ossificans - as in the question - forms a " very firm " mass

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cassdawg  Synovial cysts are also more commonly develop over a joint or tendon, whereas myositis ossificans more commonly occurs in the large muscles of the arms or legs. Location matches myositis ossificans better. +4


submitted by neonem(630), visit this page
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Aminoglycosides are nephrotoxic; nephrotoxic chemicals/drugs cause acute tubular necrosis (ATN), characterized by damage to the PCT. ATN causes the formation of brown, muddy, granular casts in the urine. The fact that this patient is a quadriplegic might be suggesting that they have a lower volume of distribution for the drug (and therefore higher blood concentrations).

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mtkilimanjaro  I would also like to add ATN is nephrotoxic ischemia and the two places in the tubule that are susceptible are the PCT (proximal straight part) and the thick ascending limb. The TAL is not labeled as a choice so that is why it has to be B (and why B is a little further down from the convoluted part) +4
mtkilimanjaro  Actually aminoglycosides might only affect the PCT idk :( +2
peridot  on p. 591 of FA 2019, it talks about ATN. The two types are 1. ischemic - affects PCT and thick ascending limb because those two areas use ATP the most (think of all the ion pumps) and 2. nephrotoxic - PCT only (I think of it as that's the first part, so it's most exposed to toxins). Aminoglycosides fall under scenario 2. +3
cassdawg  If you wanna see nephrotoxic drugs in one place, here's an image with the locations of different nephrotoxic drugs: https://media.springernature.com/lw685/springer-static/image/art%3A10.1038%2Fs41581-018-0003-9/MediaObjects/41581_2018_3_Fig1_HTML.jpg +3
corndog  Before anyone looks at @cassdawg link, consider taking some Loperamide. +6
weirdmed51  @cassdawg do you want us to be admitted in asylum before sitting for the exam? +1


submitted by m-ice(370), visit this page
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All of the features described of this patient would be expected of a 68-year-old man. Shorter, less intense orgasms, as well as increased time needed between sex could be related to a slight drop in testosterone with age. However, he continues to grow hair well (feet and toes), implying that he hasn't dramatically lost testosterone production. His prostate is slightly enlarged, which could imply benign prostatic hyperplasia, but this should not directly impact his sexual function.

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cassdawg  ^BPH threw me off: he probably does have BPH (slightly elevated PSA and diffusely enlarged prostate, common in men above 50), but BPH does not typically cause sexual dysfunction as described. BPH is more associated with urinary retention and UTI, and when it does cause sexual dysfunction urinary symptoms would be concurrently present (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1473005/ and FA2020 p654). +8
mikestix96  Normal hair growth on the toes could also imply that its not a vascular cause of decreased sexual performance (I.e. PAD with fine distal hairs) +4
bfinard1  What about the fact that it all started when he began dating the 40 year old woman 1 year ago? +
hivwizard  He says "his orgasms are shorter & he has to wait 2 or 3 hours before having sex AGAIN." when I read this I assumed that he doesn't have any psychological issues when it comes to having sex with this lady (my guy isn't scared) as well as they go multiple rounds +2


submitted by neonem(630), visit this page
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Somatostatin is normally secreted by D cells in the pancreatic islets and GI mucosa. It basically blocks everything GI-related ("encourages somato-stasis"): decreased gastric acid & pepsinogen secretion, decreased pancreatic and small intestine fluid secretion, decreased gallbladder contraction, decreased insulin & glucagon release.

Decreasing gastrin release blocks the increase of GI motility (increased GI motility is the inherent problem of diarrhea).

The drug in the question is probably octreotide.

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cassdawg  Just to add because I was trying to dissect exactly the diarrhea cause: AIDS patients can get refractory diarrhea for a variety of reasons, most commonly cryptosporidium enteritis and CMV colitis or just in general from HIV enteropathy. Octreotide has been used as a treatment for such refractory diarrhea due to the mechanisms mentioned above (https://pubmed.ncbi.nlm.nih.gov/1814331/) +4


submitted by neonem(630), visit this page
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This is acute hemolytic transfusion reaction, a type II hypersensitivity where pre-formed IgM antibodies bind to incompatible ABO antigens on donor RBCs, which causes intravascular hemolysis. Rh incompatibility, like colonelred_ said, comes more into play with Rh-compatibility of pregnancy and it is due to IgG antibodies, which more often cause extravascular hemolysis since splenic macrophages have those Fc-gamma-R receptors to bind whatever IgG has caught. Extravascular doesn't cause that hypotension, fever, flank pain associated with hemoglobinuria since the macrophages hold on to the degraded RBCs and convert it to biliverdin, which can safely be excreted by the liver.

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mousie  Could you help me with understanding why this isn't a Type I HSR? I understand that ABO incompatibility is Type II HSR but I don't know how to tell the difference between a patient who is IgA deficient and having a Type I Reaction to an infusion vs ABO incompatibility .... +16
sympathetikey  @mousie - https://imgur.com/QH5rCEX Basically, think of Type 1 HS like a normal allergic reaction (itchy, wheezing, etc.). Whereas, with ABO incompatibility you get the question's presentation. +10
medpsychosis  When it comes to Acute hemolytic transfusion reactions, they are Type II hypersensitivity and divided into Intravascular (ABO) and Extravascular (host Ab against foreign antigen on donor RBC). The differentiating factor between them is simple. Intravascular (ABO) will present with hemoglobinuria alongside all the other common symptoms (fever,hypotension, tachypnea etc.) Extravascular hemolysis will stand out with Jaundice as one of the presenting symptoms. Hope this helps! +11
cassdawg  Also just to add: Rh incompatibility causes a delayed hemolytic transfusion reaction, this reaction was immediate so it is indicative more of the ABO blood group incompatibility (FA2020 p114 has all the blood transfusion reactions) +4
ooooopss  I just wanna say God bless all of you cuzI needed this +2
drdoom  ^ linkify @sympathetikey https://imgur.com/QH5rCEX +1


submitted by passplease(37), visit this page
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Why not a tear in the sciatic nerve? especially since it radiates down to the leg

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cassdawg  My main thoughts on this is that an actual tear in the sciatic nerve is extremely difficult and further it would present with motor weakness to the muscles innervated by the sciatic nerve as well (the hamsrtings and adductor magnus, FA2020 p452). The sciatica pain that you are referring to is more common with injury to the nerve via herniated disc. +5
azharhu786  I also thought he was too young for the intervertebral disc rupture so picked sciatica tear :( +5
sexymexican888  Golijan also talks about this in his lectures he mentions how weight lifting and holding your breath increases intra-abdominal pressure and this pressure will be transferred to the CSF in the spinal cord cause a disc herniation. The pressure in the spinal cord will also go up when you do an LP and ask the patient to do valsalva or hold their breath +3


submitted by ergogenic22(401), visit this page
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Acute MI and mitral regurg (from the murmur) leads to LV failure and backflow of blood into the lungs.

This leads to increased pulmonary hydrostatic capillary pressure. This will lead to excess volume leaking from the pulmonary capillaries into the interstitial and this will manifest as pulmonary edema (crackles).

Pulmonary edema will interfere with gas exchange leading to hypoxemia.

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medstudent  Doesnโ€™t this also result in decreased alveolar ventilation since the fluid blocks air from getting to the alveoli? +5
cassdawg  ^I would agree, but I think the primary cause of hypoxemia in pulmonary edema is actually the diffusion defect rather than strictly the decrease in alveolar ventilation so the better (more NBME) answer would simply be the increased pulmonary capillary pressure as this is the root cause of all of the issues in this guy's oxygenation. +1
cassdawg  Another way of saying this is that if the defect was purely due to a decrease in alveolar ventilation, the A-a gradient would be unchanged and CO2 would be increased. However, since it is edema, the A-a gradient is increased because there is a diffusion defect, and CO2 is not significantly increased. +6


submitted by ergogenic22(401), visit this page
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Acute MI and mitral regurg (from the murmur) leads to LV failure and backflow of blood into the lungs.

This leads to increased pulmonary hydrostatic capillary pressure. This will lead to excess volume leaking from the pulmonary capillaries into the interstitial and this will manifest as pulmonary edema (crackles).

Pulmonary edema will interfere with gas exchange leading to hypoxemia.

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medstudent  Doesnโ€™t this also result in decreased alveolar ventilation since the fluid blocks air from getting to the alveoli? +5
cassdawg  ^I would agree, but I think the primary cause of hypoxemia in pulmonary edema is actually the diffusion defect rather than strictly the decrease in alveolar ventilation so the better (more NBME) answer would simply be the increased pulmonary capillary pressure as this is the root cause of all of the issues in this guy's oxygenation. +1
cassdawg  Another way of saying this is that if the defect was purely due to a decrease in alveolar ventilation, the A-a gradient would be unchanged and CO2 would be increased. However, since it is edema, the A-a gradient is increased because there is a diffusion defect, and CO2 is not significantly increased. +6


submitted by medninja(21), visit this page
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This question sounded like botulism, anybody knows why is tetanus?

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bingcentipede  I think it's because of the last sentence - asks about a defect in an inhibitory neurotransmitter, with glycine being the only possibility. I think it's one of those "here's a stem, but just look at the last sentence" questions. +6
cassdawg  This actually is not tetanus or botulism. The deficit has been present since birth. He has glycine encephalopathy, a rare disorder (https://en.wikipedia.org/wiki/Glycine_encephalopathy). Definitely could be tricked into thinking botulism but defect in "inhibitory neurotransmitter" points to glycine deficit as glycine is the only inhibitory neurotransmitter listed! +4
cassdawg  (Disclaimer that I am assuming his deficit is just a weird kind of glycine encephalopathy because normally its a disease of metabolism not receptor; but it presents with the hiccups and seizures like seen in this baby. Big thing is the last sentence as was already said) +2


submitted by medninja(21), visit this page
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This question sounded like botulism, anybody knows why is tetanus?

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bingcentipede  I think it's because of the last sentence - asks about a defect in an inhibitory neurotransmitter, with glycine being the only possibility. I think it's one of those "here's a stem, but just look at the last sentence" questions. +6
cassdawg  This actually is not tetanus or botulism. The deficit has been present since birth. He has glycine encephalopathy, a rare disorder (https://en.wikipedia.org/wiki/Glycine_encephalopathy). Definitely could be tricked into thinking botulism but defect in "inhibitory neurotransmitter" points to glycine deficit as glycine is the only inhibitory neurotransmitter listed! +4
cassdawg  (Disclaimer that I am assuming his deficit is just a weird kind of glycine encephalopathy because normally its a disease of metabolism not receptor; but it presents with the hiccups and seizures like seen in this baby. Big thing is the last sentence as was already said) +2


submitted by andro(269), visit this page
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Note: IL-12 receptor deficiency, or a defect in the Interferon Gamma receptor
Think Disseminated Mycobacterial and Fungal Infections . Also salmonella *

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cassdawg  Disseminated mycobacterial infections occur more often with interferon gamma receptor or IL-12 receptor deficiencies due to impaired ability to form granulomas (IL-12 and IFNgamma are the main cytokines involved in granuloma formation). +4
cheesetouch  FA2018 P 116 under il-12 receptor deficiency +4
cheesetouch  Also on FA18 p 102 related to Th1 response +1


submitted by andro(269), visit this page
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First step is to make the presumptive diagnosis of osteoporosis from the clinical vignette . ( The supposed subtype in our patient is postmenopausal osteoporosis)

After this the next step is to make an association with the lab findings The primary defect is a deficiency of estrogen . Normally estrogen decreases osteoclast activity by

  1. inducing apoptosis
  2. increased formation of osteoprotegerin a decoy molecule which inhibits activation of RANK receptors

Net effect of losing estrogen is increased osteoclast activity ,and in this question by extension RANK L concentration .

NOTE : ALP which is an indicator of osteoblast activity does not change/ increase in osteoporosis , as such avoid all options with an increase in osteoblast activity

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brise  But wouldn't you need osteoblasts to have RANK L? +7
cassdawg  You still have osteoblasts, they just aren't doing their "build bone" job so their primary activity is decreased. Rather, they are stimulating osteoclasts by increasing RANKL. Similar to how parathyroid hormone stimulates osteoclasts through osteoblasts --> the osteoblasts are involved but not in doing their "build bone" job; however you would never say you increase osteoblast activity with PTH even though they are necessary for PTH function. +7


submitted by hungrybox(1277), visit this page
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A: Gonadal mosaicism | Present in child, not parent โ†’ would not have family history of disease

B: Incomplete penetrance | Correct! Half of children affectd, skips a generation โ†’ AD inheritance likely.

C: Nonpaternity โ†’ Prader-Willi

D: Somatic mosaicism | Present in parent, not child โ†’ would not have family history of disease

E: Variable expressivity | Affected patients have varying disease severity โ†’ Rule out b/c mother is unaffected

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cassdawg  Also, nonpaternity can be a way of saying that the assumed biological father is not actually the father (can be a case of artificial insemination or cheating, etc.). +4
beto  In genetics, a non-paternity event is when someone who is presumed to be an individual's father is not in fact the biological father. +1


submitted by ergogenic22(401), visit this page
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Due to "contraction alkalosis" loop diuretics cause volume contraction, thats why you give them.

As a result, there is increase angiotensin II release, increase in Na+/H+ exchange in the PCT (a function of increase angiotensin II), and then increased HCO3- reabsorption, leading to alkalosis

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cassdawg  Important to remember: Loop and Thiazide diuretics cause alkalosis; Carbonic anhydrase inhibitors and potassium sparing diuretics cause acidosis (FA2020 p609) +9
cheesetouch  RE: cassdawg - FA18 p 591 +1


submitted by lsp1992(24), visit this page
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Can someone please explain what we're seeing on the histo slide? I chose the correct answer because I was thinking fungus because of the immunocompromise and neutropenia (and I thought PAS was used for aspergillus), but I don't see anything fungus-related on that slide.

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cassdawg  I think this is Blastomyces (broad based buds) where the darker pink are the blastomyces budding. Here are some similar slides: https://images.slideplayer.com/25/7691707/slides/slide_39.jpg https://www.gettyimages.co.uk/detail/photo/blastomycosis-in-the-brain-caused-by-the-high-res-stock-photography/vis303384 It could also be cryptococcus potentially (https://www.omicsonline.org/publication-images/diagnostic-pathology-budding-cryptococci-3-139-g005.png) but I think the bud bases are too broad and there is no clearing/visible capsule that cryptococcus is notable for. Either way you treat both systemic mycoses with amphotericin. +10
passplease  How did you eliminate CMV? +2
cassdawg  For me, CMV would have the characteristic "owl eye intranuclear inclusion" cells on biopsy but would be less likely to show anything in pleural fluid (i.e. thoracocentesis would not be used to diagnose CMV). Further CMV pneumonitis is an atypical/interstitial pneumonitis (diffuse patchy infiltrates on CXR, FA2020 p683) and he has a lower lobe consolidation with pleural effusion (more characteristic of fungal pneumonia). +6
shervinbd  Looks like Cryptococcus neoformans to me. +4
chaosawaits  I was pretty confident that this is Cryptococcus but the more I look at it, the more I don't know +1


submitted by bingcentipede(359), visit this page
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The two sections of the nephron most susceptible to hypoxic conditions are the 1) proximal convoluted tubule and the 2) mTAL (medullary section of the thick ascending loop of Henle)

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cassdawg  FA2020 p210 has the regions of specific organs most susceptible to hypoxic injury +4
biochemgirl22  Im thinking this is because the PCT does the most work as far as reabsorbing stuff, so probably needs the most ATP for those pumps. +3


submitted by cassdawg(1781), visit this page
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This ratio is used to determine appropriate production of lung surfactant, so this baby would not have appropriate production of surfactant if birthed at the time of the ratio calculation. It would go into neonatal respiratory distress syndrome.

TL;DR: surfactant decreases lung recoil, so the lack of surfactant in this baby will cause an increased recoil which will decrease the functional residual capacity (FA 2020 p661-662)

Surfactant is necessary to decrease surface tension of alveoli and increase compliance of the lungs (remember when the lungs have greater compliance, this makes the lungs easier to fill). Surfactant also helps to prevent alveolar collapse as the lack of surfactant allows there to be varying surface tensions between large and small alveoli (Law of Laplace), so lack of surfactant would lead to widespread atelectasis (alveolar collapse). Because surfactant serves to decrease these forces which normally favor collapse of the lung, it also serves to decrease the lung recoil.

Lack of surfactant in a baby = increased alveolar surface tension, lower compliance, more alveolar collapse, more recoil (less residual volumes)

Total lung capacity is unchanged because with enough force you can still expand the lungs to full capacity.

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geekymle  hey ya! thanks for the explanation, but i'm still not able to understand why decreased functional residual capacity. +2
cassdawg  Not sure if this will help but another way of thinking of this is that it is similar to pulmonary fibrosis with decreased compliance leading to lower functional residual capacity! The only difference is here you retain total lung capacity because it is a "reversible" compliance issue (give them surfactant) and the lungs themselves are not the issue. Also, like you said in your comment, lungs won't open up so there is a lower starting point for breathing, and thus a lower functional residual capacity (volume left in the lungs after normal expiration). +4
chaosawaits  So if FRC decreases, TLC decreases as well, which rules out E +1


submitted by metformality(15), visit this page
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This patient with a history chronic hypertension is most likely suffering from left heart failure (decreased cardiac outpout), causing the blood to back up in the lungs (Crackles are heard bilaterally, shortness of breath) and that resulting into increased afterload for the right side of the heart, raising the pressure in the right heart chambers, which get transmitted back to central vein.

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anjum  shortness of breath = Left heart failure +3
cassdawg  The way I approached the question was a little different: I realized it was heart failure and left would cause lung backup and right the venous backup. When addressing the +6
cassdawg  *the question my thinking was CO = HRxSV; in heart failure we are not pumping as much blood so lower SV (and on top of that his HR is not increased and I think the low blood pressure indicates decompensated heart failure) so CO is definitely lowered. Then CVP would have to be increased because that is how we get the edema (and backup into the venous system increases CVP). +1
chaosawaits  @cassdawg, I approached it very similarly. The best immediate indicator that this is cardiogenic shock is the pulse pressure (30 mmHg). Normal PP = 40-60 mmHg. Therefore, you know that CO has been compromised. The edema indicates that CVP (measurement of the venae cavae BP)has increased. +
an1  because this guy has crackles and ankle edema, we know that there is LHF AND RHF respectively. the most common cause of RHF is actually LHF. So crackles mean that fluid is accumulating in the lung. Where will it back up? RV and RA causing increased CVP. Crackles mean LHF, and the the LV isn't working well, the cardiac output will decrease for sure +


submitted by metformality(15), visit this page
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This patient with a history chronic hypertension is most likely suffering from left heart failure (decreased cardiac outpout), causing the blood to back up in the lungs (Crackles are heard bilaterally, shortness of breath) and that resulting into increased afterload for the right side of the heart, raising the pressure in the right heart chambers, which get transmitted back to central vein.

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anjum  shortness of breath = Left heart failure +3
cassdawg  The way I approached the question was a little different: I realized it was heart failure and left would cause lung backup and right the venous backup. When addressing the +6
cassdawg  *the question my thinking was CO = HRxSV; in heart failure we are not pumping as much blood so lower SV (and on top of that his HR is not increased and I think the low blood pressure indicates decompensated heart failure) so CO is definitely lowered. Then CVP would have to be increased because that is how we get the edema (and backup into the venous system increases CVP). +1
chaosawaits  @cassdawg, I approached it very similarly. The best immediate indicator that this is cardiogenic shock is the pulse pressure (30 mmHg). Normal PP = 40-60 mmHg. Therefore, you know that CO has been compromised. The edema indicates that CVP (measurement of the venae cavae BP)has increased. +
an1  because this guy has crackles and ankle edema, we know that there is LHF AND RHF respectively. the most common cause of RHF is actually LHF. So crackles mean that fluid is accumulating in the lung. Where will it back up? RV and RA causing increased CVP. Crackles mean LHF, and the the LV isn't working well, the cardiac output will decrease for sure +


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