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Contributor score: 140


Comments ...

 +0  (nbme13#21)

Symptoms of brain AVMS (arteriovascular malformations) include seizures. Brain avms can be found in HHT (hereditary hemorrhagic telangiectasia / Osler Weber Rendu syndrome). More info here: https://www.mayoclinic.org/diseases-conditions/brain-avm/symptoms-causes/syc-20350260 & at curehht.org


 +0  (nbme13#40)

Consult anatomy textbook/use process of elimination. (I know this isn't mind blowing, but it's what I did...)


 +0  (nbme13#22)

2 places with osteoprogenitor cells are periosteum and endosteum. Stem cells from periosteum are involved in fracture healing, whereas those in the endosteum are involved in bone remodeling. Source: https://www.kenhub.com/en/library/anatomy/histology-of-bone


 +0  (nbme13#12)

FA18 p 41. 3' end has polyadenylation signal AATAAA.


 +0  (nbme13#6)

Nitric oxide (NO) is a vasodilator, thus helping to decrease the high pressure of the pulmonary vessels. Pulmonary hypertension has excess vasoconstrictors (endothelin), and deceased vasodilators (NO, prostacyclins). FA18 p 661


 +1  (nbme16#43)

FA18 p 385. Hepatic encephalopathy treatments are lactulose (increase NH4+ generation) and rifaximin or neomycin (decrease NH3 producing gut bacteria). These treatments acidify intestinal contents (UWorld)


 +0  (nbme16#30)

FA18 p 334. Tx for pheochromocytoma is irreversible alpha antagonist (phenoxybenzamine, a1a2 blocker) followed by beta-blockers prior to tumor removal. Need to get alpha block BEFORE giving beta blockers to avoid hypertensive crisis.


 +1  (nbme15#6)

Peripancreatic fat necrosis -> calcification of mesentery


 +1  (nbme15#21)

FA18 p 501

Partial = single area of brain. Simple = consciousness intact, vs complex = impaired consciousness (IE when patient does not respond during event). Complex also presents with automatisms (lip smacking). Absence is blank stare, commonly in kids, no post-ictal confusion. Tonic-clonic has alternating stiffening and movement.


 +1  (nbme15#48)

Antianginal therapy is usually nitrates and/or beta blockers (fa18 p 312). Nitrates cause vasodilation and reflex TACHYcardia, the pt has bradycardia, suggesting beta blocker.

B1 receptor causes incr HR and contractility, suggesting the drug was antagonist of this (b1 selective antagonists = A-M olol's, FA18 p 241).

Isoproterenol is a B1=B2 sympathomimetic (FA18 p 238) so would agonize the blocked receptors, increasing HR.

An irreversible drug (like aspirin as irrev cox inhibitor) would take longer to overcome (must wait for synthesis of new cells or enzymes). The fact that the patient took 4x the normal dose and had severe effects suggests dose dependent response.


 +1  (nbme17#5)

also:

Caudate atrophy -> Huntington Disease [causes cognitive issues FA18 p 484 vs putamen has motor role]

Dentate nucleus is the most lateral deep nucleus involved in cerebellar output (FA18 p 483)


 +0  (nbme18#15)

Lose GI defense mechanism -> loss of parietal cells. ECL cells may hypertrophy to encourage acid secretion because the parietal cells are not responding to their usual signals. Zollinger-Ellison/gastrinoma causes hypertrophy of the gastric mucosa so that is also wrong.


 +1  (nbme18#9)

Dx is porphyria cutanea tarda. The deficient or defective enzyme is uroporphyrinogen decarboxylase. At the start of heme synthesis, succinyl CoA and glycine combine to form ALA (via ALA synthase), the very start of heme synthesis.


 +3  (nbme18#1)

Teratogens are most susceptible to give damage in 3-8th weeks (embryonic period - organogenesis) of pregnancy. FA p 596 (2018); teratogens section

cbreland  as @azibird stated below, the neural tube starts to form at the 3rd week and completely forms by the 4th week. Valproic acid can cause NTD, affecting their formation in weeks 3-4. +2

 +3  (nbme18#47)

Flexor digitorum PROFUNDUS tendon inserts on the DISTAL phalanges; flexor digitorum superficialis inserts on the middle phalanges. the profound go far - profundus to distal/furthest phalynx


 +2  (nbme18#47)

2 months old w/ holosystolic LLSB murmur -- ONLY holosystolic murmurs are mitral regurg, Tricuspid regurg, VSD PDA - continuous machine like murmur

isaacyo94  But this was described as a BLOWING murmur. When I hear the buzzword BLOWING murmur, I think regurg. +1
djeffs1  can someone remind me what the functional murmur would look like? +

 +2  (nbme18#10)

Even though following people ahead for 3 years may seem like a prospective cohort, that is minor and the study design with randomly assigned experimental and control groups is still a randomized clinical trial

cbreland  To add to this, a study would be observational, nothing is being assigned/added to the patients. This is too organized into groups/treatments to be a study +4

 +3  (nbme15#31)

pregnancy causes hypervolemia, and higher blood volume/flow through the heart will increase murmurs (aortic regurg.)


 +0  (nbme15#23)

Pheochromocytomas are tumors of the adrenal medulla, derived from chromaffin cells of the neural crest. In regards to the image, A is possibly the capsule allowing E to be the adrenal medulla? Here are some web images, sorry I can't solve this mystery, zoinks. https://lh3.googleusercontent.com/proxy/TtqGfP9U5W_

drdoom  ^ broken links +
cheesetouch  Sorry! I wasn't able to find a replacement. +

 +0  (nbme15#1)

Methylprednisone, a glucocorticoid, works by intracellular steroid hormone receptor signalling pathways.


 +0  (nbme15#1)

Frothy YELLOW GREEN DISCHARGE, motile organism with flagella -> dx of trichomonas vaginalis, treatment is metronidazole for patient and partner. FA2018 P158.

Trichomonas vaginalis is an STI with foul smelling green discharge, trophozoites on wet mount.

cheesetouch  intravaginal miconazole is the treatment of candida vaginitis (white cottage cheese discharge) +

 +0  (nbme15#49)

Our patient in DKA has high glucose outside her cells that will be taken up when insulin is administered. Glucokinase is the first step in glycolysis and will increase as the glucose is used. The other enzymes represent pathways that will be inactivated when insulin is given/in high glucose state (gluconeogenesis etc.) Insulin fa2018 p322


 +2  (nbme15#36)

Left dominant circulation - posterior descending artery (PDA) which supplies AV node etc is coming from the *left circumflex. Prompt says it is blocked. To get to there, the correct anatomical pathway is Left coronary artery, circumflex artery, posterior interventricular (PDA).

This can be reasoned by process of elimination too. 1- Given the Left dominant circulation, we can eliminate pathways beginning at the right coronary. 2- To get blockage at posterior of heart, we will NOT use anterior interventricular artery, so you can eliminate the 2 options listing those. 3 - The circumflex artery gives rise to the PDA, but is not the final artery in our path to the blockage (so can eliminate another two). This should give you the correct answer.

cheesetouch  FA2018 P277 heart anatomy drawing +

 +2  (nbme15#29)

Glycine is the only inhibitory neurotransmitter present. He likely has glycine encephalopathy is a rare autosomal recessive neurological disorder. Tetanus toxin - blocks release of inhibitory NT's gaba and glycine. Botulism - 'floppy baby ate honey' - inhibition of ACh release at the neuromuscular junction.


 +1  (nbme15#25)

Germline (AKA gonadal) mosaicism: mutation only in egg or sperm cell. Suspect if parent and relatives do not have the disease (or as seen here, if present in an irregular ratio/manner). FA2018 p 57


 +2  (nbme15#17)

Ampicillin (and amoxicillin and aminopenicillins) are penicillinase-sensitive penicilins. Resistance occurs when bacteria produce penicillinase (a type of beta lactamase) which cleaves the B-lactam ring. Resistance to cephalosporins occurs when bacteria produce cephalosporins (a type of beta lactamase) OR through structural changes in penicillin-binding proteins (transpeptidases). FA2018 188-189

beto  produce cephalosporinases* +1

 +1  (nbme15#42)

Acute lymphoblastic leukemia/lymphoma (ALL) is associated with Down Syndrome and most often occurs in children [FA2018 p420]. AML and ALL are increased in those with Down syndrome [p63] but median age of onset of AML is 65 years old (p420). megaloblastosis refers to megaloblastic anemia.


 +0  (nbme15#27)

A decrease in cell number means APOPTOSIS has occurred, thus the surviving tumor cells have a mutation which inhibits apoptosis

baja_blast  TGF-Beta helps regulate cellular differentiation, proliferation, and apoptosis +3

 +1  (nbme15#9) 1 tumor w/ met to liver is colon cancer Fa2018 p226
cheesetouch  sorry for a lazy answer folks! +5
docinthehouse18  Yes it was pretty obvious that it was colon cancer. However, Colon cancer is a carcinoma and only four carcinoma spread hematogenously. CRC isn't one of them. Why ISN'T the answer: tumor seeding of the abdominal cavity from the colonic tumor? Thank you! +3
cheesetouch  @docinthehouse18 Not great insight, but I think the most classic case of seeding of abdomen is omental caking in ovarian cancer (but wiki also says assoc w colon and stomach). +

 +1  (nbme17#6)

Hypokalemia is often from diuretics (EXCEPT the K sparing diuretics on the collecting tubule, SEAT [Spironolactone, eplerenone, Amiloride, Triamterene]) Hydrochlorathiazide, a diuretics acting on the DCT causes hypokalemia.

Other options: Clonidine (alpha blocker), Lisinopril (ACE-inhibitor), Metoprolol (beta blocker), Triamterene (K sparing diuretic).


 +2  (nbme17#36)

Glucocorticoids inhibit Nfkb, suppress both B and t cell function by decreasing transcription of many cytokines. Induce T cell apoptosis FA 2018 P120


 +0  (nbme17#32)

FA 2018 p 290 - treat 3rd degr heart block with pacemaker

srmtn  FA2019 p293 +

 +0  (nbme17#50)

odds ratio for the exposure variable (aniline dye) = (yes cancer and yes dye / yes dye) / (no cancer and yes dye / yes dye) = (250/250) / (50/150) = 3

cheesetouch  FA 2018 P 254 +1
cheesetouch  oops messed up the denominator a bit. 50/150 = (no cancer yes dye / no cancer no dye) +

 +1  (nbme17#1)

Sensitivity of 99% means that almost all TA will have high ESR. (Sn = tp/(tp+fn) -> low False negative). HOWEVER, a specificity of just 60% means high ESR can indicate MANY OTHER disease processes. In a test with low specificity, more tests should be done to confirm diagnosis.


 -6  (nbme17#14)

Azoles (including itraconazole) and omeprazole are both P450 inhibitors. (p450 interactions FA2018 P247, azoles FA2018 p199.

shieldmaiden  They inhibit different isoenzymes +

 +0  (nbme17#27)

The unaffected person will have the alleles from their parents not present in the diseased people. This is alleles 2 and 3.





Subcomments ...

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hiTs eqtiusno is ikgsan rof teh ualscrva pylspu fo eht ryhtpdroaia gsdnal. ahtT wludo be eth nfieorri oiyrdht stirr,eea hhcwi arsie mofr hte trcirahovelyc .urktn

weenathon  I originally chose vein because I was thinking maybe the hormone release couldn't be carried to the body anymore, but looking back the working of "moderate hemorrhaging" and vessels requiring ligation is what implies it's an artery. Just throwing that out there in case you thought like I did. +4  
cheesetouch  if you were clueless like me (well I knew artery but..), picking one with 'thyro' in the name when discussing a thyroid surgery is a good guess :) +6  
cbreland  I'm really out here picking one of the answers with vein +  


submitted by trazobone(35),

SMH I was thinking alcoholic B12 loss of vibratory, so obvious now he has ALS. Hyperreflexia UMN sign, fasciculations LMN sign. And common cause of death is due to aspiration pneumonia because of dysphagia (LMN deficit). FA 2018 p 514

trazobone  Sorry dysphagia (UMN deficit) +  
trazobone  SMH I was thinking alcoholic B12 loss of vibratory, so obvious now he has ALS. Hyperreflexia UMN sign, fasciculations LMN sign. And common cause of death is due to aspiration pneumonia because of dysphagia (UMN deficit). FA 2018 p 514 +  
cheesetouch  UMN vs LMN is FA18 p 513 also! +  


submitted by trazobone(35),

If anyone else is on the dumdum boat and didn’t know what a paranganglioma was: a neuroendocrine tumor that begins in nerve cells, closely related to a pheochromocytoma

cheesetouch  Mayo clinic says 2 out of 1 million people have a paraganglioma. Talk about a zebra! +1  


Diagnosis: strawberry hemangioma

Heme = blood -ang- = vessel -oma = benign mass

A benign tumor of capillaries, therefore the origin is endothelium

cheesetouch  NOTE: Endothelium derived from mesoderm. (I was mis-reading this as endoderm). +  


submitted by ergogenic22(321),
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I lieeveb atht teh uqniseot is gusesngtig het titanep has a nteaholm oo.vreeds

Firts Aid 2108 gape FE2lM"po:sO7—betizh inii ahololc yrdnehsaeegdo and is na anoitedt For dovOeerss of olaenMth ro yEheentl ."olglcy

hTe nsraeo I am enrusu si that iwipaekdi asttes tsom iatnp inehnrst ear stekeno ro sroahrbndoyc

lae  that's correct, I don't know about what the thinner has but the clinics is methanol toxicity for sure +1  
cheesetouch  FA18 p 576 mentions AGMA causes include methanol. It also mentions formic acid. Formic acid is VERY structurally similar to acetone (a chemical in paint thinner and nail polish remover). [Sorry this isn't a great answer, but it's a thought...] +  


submitted by cassdawg(1165),

Neural crest cells migrate to form the aorticopulmonary septum and abnormalities associated with neural crest migration in the heart include tetrology of fallot, transposition of the great arteries, and persistent truncus arteriosus. Fusion of the aorticopulmonary septum with the muscular ventricular septum is what forms the membranous septum, so patients with a persistent truncus arteriosus will have VSD as well. (FA2020 p280)

i_hate_it_here  Neural Crest derivatives: Melanocytes Odontoblasts Tracheal cartilage Enterochromaffin cells Leptomeningies (pia & arachnoid) PNS Adrenal medulla Schwaun cells S aorticopulmonary Septum Endocardial cushions (defects resulting in asd & vsd) Skull bones FA2020 pg 613 +  
i_hate_it_here  MOTEL PASSES +1  
cheesetouch  fa18 p 298 Persistent truncus arteriosus +  


submitted by cassdawg(1165),

Polyarteritis nodosa is a medium vessel vasculitis associated with different stages of transmural inflammation with fibrinoid necrosis of vessels. [FA2020 p314]

Because this is a vasculitis that affects medium vessels, it can affect the arteries supplying the muscles and thus cause segmental ischemic necrosis from loss of blood supply.

radzio1  I thought that segmental is a key word for Burgers dz. +1  
radzio1  *Buerger +  
feochromocytoma  Beurger is characterized by segmental thrombosis with nerve involvement. +2  
cheesetouch  So he has both PAN and Buerger's? +  
pakimd  polyarteritis nodosa is characterized by segmental (different stages) of transmural inflammation with fibrinoid necrosis causing narrowing of vessel lumen and increased risk of thrombosis leading to tissue ischemia/infarction FA2020 pg314 +  
shieldmaiden  The problem in Buerger is segmental thrombosis while PAN is ischemia from immune complexes with hepatitis antigens and it is also segmental (a string of pearls) +  


submitted by bingcentipede(260),

Kid had a viral URI then took aspirn -> Reye syndrome, a hepatic encephalopathy. There is increased ammonia production because of the liver damage, leading to hyperammonemia. This gets to the brain, is ocnverted to glutamine (an osmolyte). This causes the brain swelling.

It's not E) viral encephalitis because it implies the virus is directly causing the encephalitis. Instead, the viral infection -> aspirin -> liver damage -> ammonia -> crosses BBB -> converted to glutamine -> draws in water -> cerebral edema

https://step1.medbullets.com/gastrointestinal/107080/hepatic-encephalopathy

furqanka  /\ sorry .. https://onlinelibrary.wiley.com/doi/full/10.1111/jgh.14408 figure 1 +1  
cheesetouch  FA18 p 384 +  


submitted by cassdawg(1165),

Vinblastine works by binding tubulin and inhibiting microtubule formation. This inhibits cell division.

Basically, this question is asking which of the following cell types is nondividing/would not need functioning microtubules.

Enterocytes in crypts (which divide to replace intestinal epithelium(, keratinocytes of the stratum basale (which divide to to replace skin), and erythroblasts (blasts are stem cells) are all dividing cells and thus could be affected by vinblastine. Cortical thymocytes are also dividing cells, as they will divide to create progeny T-cells through the process of T-cell maturation.

Thus, the only non-affected cell is ventricular cardiomyocytes.

the_enigma28  Cortical thymic epithelial cells (cTECs) [aka cortical thymocytes] form unique parenchymal cell [& therefore proliferating] population of the thymus which critically contribute to the development of T cells +3  
cheesetouch  Pathoma Ch 1.1 mentions permanent tissues include: cardiac muscle, skeletal muscle & nerve - only can grow by hypertrophy. +2  


submitted by daddyyikes(0),
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it is rcahcto iamre thoto essidae as ti si eedthinir and whti mablanro yeilmn ,aehhst ooft prd,o maremh toe .tec

cheesetouch  fa18 p 508 +  


submitted by aoa05(27),

here are partial clinical manifestations of the right oculomotor nerve palsy:  the right pupil is 6 mm and nonreactive to light, and adduction of the right eye is impaired. The oculomotor nerve exits midbrain through the interpeduncular fossa and goes between the beginning of the posterior cerebral and superior cerebellar arteries. Rapture of an aneurysm in the posterior communicating artery near the beginning of the posterior cerebral artery may compress the oculomotor nerve and affect its function

medstudent  FA 2020 P. 516 +1  
baja_blast  FA 2019 p. 529. +  
cheesetouch  FA18 p 525 CN III damage +  


submitted by cassdawg(1165),

The facial nerve exits the skill via the internal acoustic meatus where it will traverse through the inner ear cavity (FA2020 p505 and 506). The facial nerve also innervates the muscles of facial expression and thus would cause her ipsilateral facial weakness (facial nerve lesions p532).

feochromocytoma  Also known as the internal auditory meatus in some texts. +  
cheesetouch  FA18 p 489 +  


submitted by hiroshimi(7),

Among these, only amphetamine is a stimulant drug. Stimulants intoxication usually characterize by mydriasis, high BP, high HR, and one way to detox is through activated charcoal. Pt may also experience paranoia which can be mistaken for schizophrenia. Another drug that has the same presentation is cocaine since they are both stimulants.

Barbiturate, benzo, and opioids characterized by respiration depression, miosis (for opioid). Marijuana intoxication with sx of hyperphagia and probably other sx but I forgot.

cheesetouch  FA18 p 556 - CNS stimulants/amphetamines +  


submitted by cassdawg(1165),

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)

topgunber  physostigmine because its liposoluble and has central effects as compared to neostigmine +3  
cheesetouch  FA18 p 237,236 +1  
topgunber  its you isnt it @cheesetouch +  


submitted by cassdawg(1165),

Peutz-Jeghers syndrome is an autosomal dominant syndrome associated with hyperpigmented macules on the mouth, lips, hands, and genetalia as well as increased risk of breast and GI cancers. [FA2020 p387]

This patient presents with the characteristic hyperpigmented macules as well as positive occult blood test which could be indicative of an underlying GI malignancy. Peutz-Jeghers is also associated with numerous hamartomas throughout the GI tract which could be associated with the patient's general GI symptoms due to their ability to cause blockage.

Other answers:

  • Cowden disease - multiple hamartoma syndrome that increases risk of breast, thyroid, uterine, and other cancers; it is not associated with the hyperpigmented macules
  • Gardner syndrome - familial adenomatous polyposis + osseous and soft tissue tumors
  • Muir-Torre syndrome - rare hereditary autosomal dominant cancer syndrome thought to be a subtype of HNPCC (Lynch syndrome)
  • Neurofibromatosis - not associated with GI issues and typically have a very different presentation (FA2020 p525) - NF1 = cafe-au-lait spots, lisch nodules, pheochromocytoma, seizures, cutaneous neurofibromas, etc.; NF2 = bilateral vestibular schwannomas, juvenille cateracts, meningiomas, ependymomas
cheesetouch  FA18 p 381. Great answer cassdawg! +  


submitted by aoa05(27),

First, the boy had ophathalmoplegia (eye muscle problem) and hypotonia (muscle weakness), indicating that he had muscle related problems. Second, all the problems appeared to come from his mother’s side and the symptoms from different individuals of the family appeared to be very heterogeneous and diverse. All these strongly suggest heteroplasmy, a mitochondrial genetic disease, which is known to show varying degrees of expressivity owing to heterogeneity in genetic mutations in mitochondria. All the mitochondria of one person are inherited from mother’s side (from fertilized eggs) and are different from nuclear chromosome inheritance mechanism. Heteroplasmy is caused by the fact that in each human cells, there are several hundreds mitochondria. In different mitochondria, they may contain different genetic mutations. During genetic transmission, different mitochondria may end up in different eggs / fertilized eggs, leading to mitochondrial genetic disease in the offspring with varying degrees of expressivity owing to heteroplasmy

How to exclude other possibilities: In the narrative, there are genetic diseases two generations in a row in the family. Thus, it is not recessive disease. It came from his mother’s side but affected both sexes. It does not look like a penetrance issue, Additional information - MERRF syndrome (or myoclonic epilepsy with ragged red fibers) is a mitochondrial disease MERRF syndrome affects different parts of the body, particularly the muscles and nervous system. The signs and symptoms of this disorder appear at an early age, generally childhood or adolescence. The primary features displayed on a person with MERRF include myoclonus, seizures, cerebellar ataxia, myopathy, and ragged red fibers (RRF) on muscle biopsy, leading to the disease's name. Secondary features include dementia, optic atrophy, bilateral deafness, peripheral neuropathy, spasticity, or multiple lipomata. Mitochondrial disorders, including MERRFS, may present at any age

nbmeanswersownersucks  I agree with everything you said though I don't think the disease in the question is MERRF. unless I misunderstood you and you weren't saying it was MERRF but were just describing an example of a mito disease? +7  
nbmeanswersownersucks  I think it is more in line with MELAS d/t the lactic acidosis and stroke +4  
i_hate_it_here  Username checks out +  
cheesetouch  FA18 p 57 Heteroplasmy and p59 MELAS syndrome +  


COPII = RER to Golgi

COPI = Golgi to RER

HINT: 2 steps forward, 1 step back

If the COPII protein is mutated, then the vesicles and their contents build-up in the RER. Hence, the right answer is dilated RER.

cheesetouch  FA18 COP II p 47 +  


submitted by bingcentipede(260),

Puberty (Tanner stage II) begins at its EARLIEST at... -8 years old for a girl (thelarche) -9 years old for a boy

cheesetouch  FA18 p 619 +  
dermgirl  FA2020 p.637 +  


submitted by bingcentipede(260),

This is a peri-menopausal woman experiencing the typical symptoms of hot flashes and irregular periods. Decreased estrogen/progesterone production leads to vaginal atrophy and negative feedback onto the anterior pituitary, leading to increased FSH and LH hormones.

baja_blast  Menopause on FA2019 p. 622 +  
cheesetouch  FA18 Menopause p617 +  
dermgirl  Menopause on FA2020 p. 636 +  


submitted by motherhen(40),

In other words, what is the active product of the thyroid gland that is needed for normal development? Only thyroxine, iodine and thyroglobulin are in the thyroid gland. Of these, thyroxine is the active hormone produced that would affect development.

cheesetouch  *refuting thyroglobulin * Wikipedia: Thyroglobulin (Tg) acts as a substrate for the synthesis of the thyroid hormones thyroxine (T4) and triiodothyronine (T3), as well as the storage of the inactive forms of thyroid hormone and iodine within the follicular lumen of a thyroid follicle +  


submitted by medninja(18),

MEN 1--> Pituitary tumors, pancreatic endocrine tumors (zollinger ellison or gastrinoma) and parathyroid adenomas.

nbmeanswersownersucks  the question hints at a possible parathyroid adenoma with her history of 2 episodes of renal calculi. +4  
feochromocytoma  Yup, also as a tip for next time, if you see that a patient has some sort of pancreatic cell tumor, such as Zollinger in this case, look for other MEN 1 associated findings. +  
cheesetouch  FA18 347 +1  


submitted by cassdawg(1165),

This is eclamsia because of the hypertension in pregnancy with symptoms of end-organ damage and failure combined with siezures (FA2020 p643).

None of the other answers are consistent with the presentation. Epilepsy alone does not cause the symptoms of end organ damage (elevated liver enzymes, lactate dehydrogenase, and inability to urinate), renal disease alone likewise would not cause the combination of symptoms. Sepsis and septic shock causes hypotension not hypertension as seen in this patient. There is no specific drug toxidrome that matches the combination of symptoms.

the_enigma28  Its HELLP syndrome. Hemolysis, Elevated Liver enzymes, Low Platelets. Eclampsia was the closest answer. +8  
i_hate_it_here  HEELLP syndrome is a condition that presents with preclampsia and eclampsia is just preclampsia with seizures +  
cheesetouch  FA18 625 HELLP +  


submitted by zincy7(17),
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  • nBgirnu ibAndloam Pina ohrus aetrf engita = tsaGcir ucrel
  • kBcal sotlso fro 2 asyd = ???
  • feoRytrcar to COT idscnatA nda H2 orlescBk
  • giwtSaen nad Low PB
  • rncaiPecat ssMa = tsom kyllei TGMOASNRIA
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Neo:t Yuo odlush ieresv het tuf,oninc asinmoilu,tt dan iest fo leasree rof eahc fo the ehmorson nteodienm sa llew

ERN:REFEEC nrioesolZlgnillE- nyomSerd

bingcentipede  Black stool because blood in the GI tract? +1  
passplease  I was tempted to pick insulin, because of the orthostatics and sweating that could resemble hypoglycemic episodes. Why are those present in a gastrinoma? +3  
deberawr  @passplease it's possible that increased gastrin -> peptic ulcers -> perforation -> shock -> sympathetic nervous system overload -> sweating and hypotension +  
jsanmiguel415  Black stool = melena = bleeding above the ligament of trietz from ulcers +  
rina  @passplease according to amboss gastrinomas can cause steatorrhea and malabsorption, in addition to anemia from GI bleeding. that might explain the light headedness and low-ish bp. +  
jj375  Zollinger Ellison Syndrome --> causes duodenal ulcers that are bleeding causing melena and the low blood volume (symptoms of light headed and low BP). I would guess that sweating is from what @deberawr said of the increased sympathetics from the low blood volume +1  
cheesetouch  FA18 347 zollinger ellison +  


The patient can only achieve erections via direct stimulation aka touch. The pudendal nerve provides somatic innervation and thus sensation to the penis as well as the perineum. A purely sensory stimulated erection involves a reflex arc between the pudendal afferent nerves and efferent sacral parasympathetic nerves (aka pelvic splanchnic nerves).

cheesetouch  Fun Facts: pudendal can be blocked for childbirth anesthetic using ischial spine as landmark. Injury to this nerve can cause fecal or urinary incontinence. Is sensory to perineum, motor to external urethral and anal spinchters. +  
cheesetouch  Obturator nerve is incorrect - the word obturator means "to close" and it innervates thigh adductors. +  
cheesetouch  Genitofemoral nerve is also incorrect - sensory to scrotum/labia majora and medial thigh, motor for cremasteric reflex. FA 18 442-443 +  


The patient can only achieve erections via direct stimulation aka touch. The pudendal nerve provides somatic innervation and thus sensation to the penis as well as the perineum. A purely sensory stimulated erection involves a reflex arc between the pudendal afferent nerves and efferent sacral parasympathetic nerves (aka pelvic splanchnic nerves).

cheesetouch  Fun Facts: pudendal can be blocked for childbirth anesthetic using ischial spine as landmark. Injury to this nerve can cause fecal or urinary incontinence. Is sensory to perineum, motor to external urethral and anal spinchters. +  
cheesetouch  Obturator nerve is incorrect - the word obturator means "to close" and it innervates thigh adductors. +  
cheesetouch  Genitofemoral nerve is also incorrect - sensory to scrotum/labia majora and medial thigh, motor for cremasteric reflex. FA 18 442-443 +  


The patient can only achieve erections via direct stimulation aka touch. The pudendal nerve provides somatic innervation and thus sensation to the penis as well as the perineum. A purely sensory stimulated erection involves a reflex arc between the pudendal afferent nerves and efferent sacral parasympathetic nerves (aka pelvic splanchnic nerves).

cheesetouch  Fun Facts: pudendal can be blocked for childbirth anesthetic using ischial spine as landmark. Injury to this nerve can cause fecal or urinary incontinence. Is sensory to perineum, motor to external urethral and anal spinchters. +  
cheesetouch  Obturator nerve is incorrect - the word obturator means "to close" and it innervates thigh adductors. +  
cheesetouch  Genitofemoral nerve is also incorrect - sensory to scrotum/labia majora and medial thigh, motor for cremasteric reflex. FA 18 442-443 +  


submitted by bingcentipede(260),

Clomiphene is a SERM that antagonizes estrogen receptors in the hypothalamus.

If estrogen is antagonized there, there is decreased negative feedback to improve FSH and LH release to stimulate ovulation. This is very important in PCOS and other disorders with decreased fertility.

notyasupreme  I guess I wasn't sure because it said FSH and LH levels were normal, so I assumed the problem was with progesterone. But I thought too deep into it and should've just went with my gut. +1  
feochromocytoma  Clopmiphene is usually the answer for infertility with NORMAL anatomy and NORMAL appearing labs +1  
drdoom  very nice +  
cheesetouch  FA18 p 637 +  
sexymexican888  Yeah I made the same mistake by choosing progesterone BUT they are used for contraception (pill, IUD etc) and for the PROGESTIN challenge EXCLUDES (if +withdrawl bleed its hormonal PCOS etc) uterine bleeding due to anatomic defects (which will have no withdrawal bleeding i.e asherman) so as far I know its not used as fertility treatment +  


This seems like NADPH oxidase deficiency, as the patient has history of multiple cutaneous abscess with Staph aurues during past 9 months. Therefore, a catalase positive organism is the likely cause, besides microbiological characteristics befitting Nocardia

cheesetouch  FA18 p 117 chronic granulomatous disease (NADPH oxidase deficiency), FA18 p139 Nocardia +  


submitted by acerj(8),

So, this is one of those few calculation problems that you might see on Step 1.

The vignette points to 3-day history of vomiting/diarrhea, holding nothing down, and little urine output. Also, from the BP readings, this guy is orthostatic pointing towards volume depletion.

However, looking at the Serum labs, he has azotemia with a BUN of 50mg/dL. In this case, AKI (ATN in the answers) and volume depletion should be your top two.

To differentiate, you could calculate FENa, the fraction of Na excreted.

FENa = ( [Na in the Urine] * Flow Rate of the Urine / [Na in the Plasma] ) / ([Cr in the Urine] * Flow Rate of the Urine / [Cr in the Plasma]

Simplifying to cancel out the Flow Rate of the Urine leaves us with:

FENa = ([Na in the Urine] * [Cr in the Plasma]) / ([Na in the Plasma] * [Cr in the Urine])

For this problem: FENa = [10mEq/L] * [2.2mg/dL] / ([146mEq/dL]*[19mg/dL]) = 0.007 or 0.7%

That points definitively to prerenal AKI and volume depletion.

ibpstepprep  more specifically , a specific gravity of greater than or equal to 1.030 = frank dehydration = volume depletion. I don't think you have to calculate the FeNa, knowing urine sodium is less than 20 indicates prerenal failure ( FA 19 590). The key to this problem is the specific gravity +1  
cheesetouch  I didn't do any calculation, just went off patient's history, tried to think of how the Na is barely high (146 when NBME normal is up to 145), what the heck would make uric acid high in that history, plus no RBCs in urine. +  
sexymexican888  FA 2020 P 601: You don't have to calculate FENa, you can just look at the sodium 10 mEq/L. In pre-renal azotemia urine Na is <20 mEq/L meaning the tubules are patent and Na is being reabsorbed properly, even more than usual since its sensing volume depletion. IN CONTRAST intra-renal failure will have a urine Na >40 mEq/L bc the renal tubules are damaged (ATN) and cannot reabsorb Na properly. +  
sexymexican888  FENa is the same concept . pre-renal azotemia ->FENa <1% -> Na is being reabsorbed -> Kidney is healthy and working . . . Intrinsic renal failure -> FENa >2% -> Na is NOT being reabsorbed properly -> Kidney is NOT healthy +  
sexymexican888  also BUN/Cr ratio: 50/2.2 ~ 25 in pre-renal azotemia BUN/Cr >20 (kidney's capacity to reabsorb is intact) if it was ATN BUN/Cr ratio would be <15 (kidney is fucked up cant reabsorb urea properly) +2  
ddaddy  Calculation is a waste of time. Hx of vomiting/diarrhea is all that is needed +1  


Hello, i think it is Streptococcus viridans; coccus in chains and normal oral flora. Alcoholics can get aspiration pneumonia, which can evolve to a pulmonary abscess. FA2020 p146. https://www.atsjournals.org/doi/pdf/10.1164/ajrccm.156.5.97-03006

cheesetouch  fa18 p 136 +  


submitted by cassdawg(1165),

The burnt almond smell and noncyanotic dyspnea is characteristic of cyanid poisoning. Cyanide poisoning is treated with nitrites because nitrites oxidize hemoglobin to form methamoglobin which binds cyanide, allowing less toxicity. Thiosulfate is often added to increase renal excretion as thiocyanate. Cyanide toxicity may also be treated with hydroxycobalmin, which binds cyanide.

FA2020 p667 has differentiation of cyanide from CO poisoning.

drippinranch  is there a circumstance where you would treat cyanide poisoning first with hyperbaric oxygen before hydroxy/nitrates/thiosulfate? +1  
prosopagnosia  If the patient had concomitant carbon monoxide poisoning, then I think the hyperbaric oxygen would help. But in order to reverse cyanide poisoning, hyperbaric oxygen will not help because the cells are unable to use oxygen since the cyanide directly inhibits oxidative phosphorylation. +1  
i_hate_it_here  Another thing to know about this is that unlike with CO poisoning, your O2 saturation of hemoglobin, total O2 content, and oxygen-hemoglobin dissociation curve would all be normal. FA2020 pg: 666 +1  
trazobone  Thank you i love it here +  
cheesetouch  FA18 p 648 +  


submitted by cassdawg(1165),

This man has acute intermittent porphyria which is a deficiency in porphobilinogen deaminase because: (FA2020 p425)

  • Painful abdomen
  • Port-wine colored urine (burgundy urine)
  • Precipitated by drugs - triggered by TMP/SMX
  • Psychological disturbances - irrational behavior
  • Family history
  • Increased 5-ALA and porphobilinogen which are the two prior substances in the heme synthesis pathway that would be backed up
cheesetouch  fa18 p 413 +1  


submitted by trazobone(35),

Cool and pale extremities rules out distributive causes (neurogenic, anaphylaxis, septic).

Hypovolemia would describe a process of volume loss bleeding (or dehydration) and would not explain the crackles or jugular venous distention.

Don’t be thrown off by the normal heart sounds. I am getting real good at this descrambling thing.

cheesetouch  JSYK, if it shows scrambled to one person doesn't necessarily mean it does to another. And wouldn't this possible show scrambled too to them :P? +  
trazobone  No because I’ve seen a trend where they only descramble comments posted more than a year ago. Everything that’s I’ve seen commented last month or within the last couple of months is unscrambled. But this is only a working theory lol +2  


submitted by cassdawg(1165),

The stem describes tenderness in the anatomical snuffbox ("radial aspect of the wrist between the abductor pollicis longus and extensor pollicic brevis"). This is indivative of a fracture of the scaphoid bone. One of the more common complications is avascular necrosis of the proximal scaphoid bone. [FA2020 p449]

randi  FA2019 p439 +  
cheesetouch  FA18 435 +  


submitted by andro(189),

The question essentially wants you to make a distinction between Pubertal Gynecomastia and Pathological Gynecomastia

Pubertal gynecomastia

  1. may be unilateral or bilateral
  2. tender or nontender
  3. found in 50 % of adolescents and typically resolves by the age of 17 , and as such patients require little more than reassurance

This Patient however is already above the age of 17( rule out reassurance !) Of the possible causes of pathological gynecomastia , anabolic steroid use is a very likely option based on the description provided

trazobone  See i assumed this was a “how to be a more empathetic physician” question, so i said reassurance. But i guess not putting reassurance makes sense bc it implies everything is normal +4  
cheesetouch  @Trazobone I think it's just one of those "suspect everyone until proven trustworthy/otherwise" questions :P +1  


submitted by cassdawg(1165),

FA2020 p 612 has early fetal development. Here are the explanations for the answers:

Basically, even without knowing all the exact days of development, most answers can be eliminated based on having the events in the incorrect order or having an incorrect aspect about development (i.e. the syncytiotrophoblast forms concurrent with the cytotrophobast, 3 germ layers are present after gastrulation, the embryo is never truly resistant to teratogens after implantation, the sclerotome forms from somites so somites have to come first).

Here is a general overview of the first three weeks of development after fertilization.

Here is another one if that doesn't do it for ya.

cheesetouch  FA18 p 594, 599 (syncytiotrophoblast) +  


submitted by cassdawg(1165),

This is a partial mole because of the presence of fetal parts. Complete moles have no fetal parts, partial moles have fetal parts(PARTial = fetal PARTs). (FA2020 p642)

cheesetouch  FA18 p 622 +  


submitted by cheesetouch(140),

Pheochromocytomas are tumors of the adrenal medulla, derived from chromaffin cells of the neural crest. In regards to the image, A is possibly the capsule allowing E to be the adrenal medulla? Here are some web images, sorry I can't solve this mystery, zoinks. https://lh3.googleusercontent.com/proxy/TtqGfP9U5W_

drdoom  ^ broken links +  
cheesetouch  Sorry! I wasn't able to find a replacement. +  


submitted by cassdawg(1165),

Premature infants have a lack of surfactant which decreases compliance of the lungs and increases the lung elastic recoil (FA2020 p665).

The high surface tension is the main contributor to elastic recoil in the lung of a neonate. Because the surface tension is high due to lack of surfactant, recoil is also high, and the lungs and alveoli have more tendancy to collapse.

cassdawg  This has to do with the Law of Laplace and how this collapsing pressure is related to surface tension (FA2020 p661) +  
cheesetouch  FA18 p 643 +  


submitted by ergogenic22(321),
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ueD to nrant"cctoio losopalaol ik"s educirtsi uscea mlovue cn,ittaoornc ttash hyw uoy evig .mteh

As a tersul, rhtee si inceasre iinetsnoang II ees,alre aceeinrs in H+aN+/ hexecang in the TCP a( inonufct of nceseira tnningiaeso )II, and nhet crsneieda -C3OH osirnortbepa, ineadlg to liakosasl

cassdawg  Important to remember: Loop and Thiazide diuretics cause alkalosis; Carbonic anhydrase inhibitors and potassium sparing diuretics cause acidosis (FA2020 p609) +5  
cheesetouch  RE: cassdawg - FA18 p 591 +  


submitted by cassdawg(1165),

A furuncle is a boil, typically caused by staphylococcal infection. Thus, it can be deduced that the food poisoning is due to staphylococcus aureus, which forms a heat stabile enterotoxin not destroyed by cooking. Ingestion of the preformed enterotoxin causes vomiting.

i_hate_it_here  Oh, i guess I thought the preformed toxin would lead to hella diarrhea and then shock... silly me +  
cheesetouch  I think the right answer might be more related to letting a meatloaf with raw hamburger sit for 12 hours at room temp. E coli the hamburger toxin! (although that's associated with uncooked meat and 350 for an hr should be plenty of time to cook it unless it's real thicc) +  


submitted by cassdawg(1165),

Carotid sinus massage is a mechanism of inducing activation of the parasympathetic system. This is because the baroreceptors in the carotid sinus.

Caortid sinus massage --> activation and increased firing of baroreceptors --> transmission to solitary nucleus via glossopharyngeal nerve --> decreased sympathetic output and increased parasymapthetic output v --> increased AV node refractory period and decreased HR

FA2020 p296

cheesetouch  FA18 p 291 +  
hecticsurreyguy  Want to reduce the heart rate while maintaining cardiac output - digitalize the patient (give them digoxin). Digoxin: 1. increase vagal stimulation of the AV node, thereby reducing heart rate. = "Increased cardiac parasympathetic activity" 2. increase the contractility of the heat. This way alothough you're reducing the heart rate, you're maintaining cardiac output. +  


submitted by cassdawg(1165),

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)

cheesetouch  FA18 p for list of brain vulnerable to ischemia is P 496. Hippocampus, neocortex, cerebellum (purkinje cells), watershed areas. +  


submitted by deberawr(5),

"Histone deacetylase: An enzyme that removes acetyl groups from histone proteins, which exposes positively-charged lysine residues. As a result, negatively-charged DNA binds more tightly to the histone, which prevents transcription." - Amboss

deberawr  note the question regards histone deacetylase INHIBITORS, but it affects transcription nonetheless +  
cheesetouch  Anyone have any thoughts as to why post-translational processing is incorrect? Post translational modifications include acetylation, so I was thinking processing would be analogous. +  


submitted by ploy901(9),

The mainstay therapy for Hodgkin disease (aka Hodgkin lymphoma) is radiation. This can induce DNA mutations in any bone marrow nearby. If the mutation knocks out genes related to apoptosis, proliferation, DNA proofreading, or the like, malignancy could occur over time.

ploy901  Also note that alkylating chemotherapeutic drugs increase the risk for leukemia and lymphoma years down the line too +4  
cheesetouch  AML section mentions risk factors incl radiation and alyklating chemo (FA18 p 420) +  


submitted by cassdawg(1165),

Beta-thalassemia minor is the only potentially asymptomatic disease of the answer choices. It is asymptomatic because even though it leads to underproduction of the beta chain, there is compensation by increased HbA2. It causes a microcytic anemia, as seen (FA2020 p418).

  • Aplastic anemia would have decrease in every cell type and would more likely be symptomatic
  • Folic acid deficiency and B12 deficiency both cause macrocytic anemia, and B12 would have added neuroligic deficits
  • Sickle cell disease would definitely be symptomatic and she would have history of the disease. It also causes a hemolytic anemia. Sickle cell trait could be asymptomatic.
cheesetouch  FA18 p 407 +  


submitted by cassdawg(1165),

The -navirs are protease inhibitors, so a mutation in protein processing would cause resistance.

radzio1  in FA p203 it literally says Protease Inhibitors act by inhibiting maturation and assembly. So thats what I picked. Why is protein processing more appropriate? +2  
radzio1  in FA p203 it literally says Protease Inhibitors act by inhibiting maturation and assembly. So thats what I picked. Why is protein processing more appropriate? +  
kaf  maybe packaging means sending out of the cell? +  
pakimd  on pg 203 of first aid it says protease inhibitors inhibit HIV-1 protease which cleaves polypeptide products of HIV mRNA into their functional parts; proteases are responsible for cleaving and processing proteins made from HIV RNA transcript into functional parts and protease inhibits this process by inhibiting proteases responsible for processing proteins that are made from HIV mRNA +  
pakimd  on pg 203 of first aid it says protease inhibitors inhibit HIV-1 protease which cleaves polypeptide products of HIV mRNA into their functional parts; proteases are responsible for cleaving and processing proteins made from HIV RNA transcript into functional parts and protease inhibits this process by inhibiting proteases responsible for processing proteins that are made from HIV mRNA +  
pakimd  protease inhibitors* inhibit proteases +  
pakimd  and then those functional proteins are assembled and packaged into virions to be released and infect other T cells +  
pakimd  if you look at the illustration on pg 201 of FA youll see that they say that protease inhibitors inhibit proteolytic processing +1  
cheesetouch  in a UW question I did, it said that protease inhibitors inhibit gag-pol cleavage, which would probably be considered a form of processing. gag -> p24 capsid and p17 matrix proteins pol -> reverse txase, aspartate protease, integrase pakimd makes a great point above about the img on 201. I think this is just kind of a crappy question LOL +  
whk123  [Check here the image says that, sketchy pharma mentioned regarding pol gene too in regard of navirs] (https://basicmedicalkey.com/wp-content/uploads/2017/02/image01621.jpeg) => Here it comes +  


submitted by pakimd(14),

@docinthehouse18 yes colon cancer spreads to distant organs via lymphatics e.g. to the lungs but the reason why the most common location of colon cancer metastasis is the liver is because of the unique anatomic situation with regards to portal venous system. so colon cancer spreads to the liver hematogenously via portal venous system but otherwise spreads to distant sites via lymphatics. the question asks the route of metastasis to the liver and tumor seeding of the abdominal cavity from the colonic tumor will not cause mets in liver. 4 carcinomas that spreads hematogenously only and only spreads via blood.

cheesetouch  4 hematogenously spreading cancers (pathoma ch3): RCC (renal vein) HCC (hepatic vein) Choriocarcinoma Follicular ca of the thyroid +1  


submitted by cheesetouch(140),
1 tumor w/ met to liver is colon cancer Fa2018 p226
cheesetouch  sorry for a lazy answer folks! +5  
docinthehouse18  Yes it was pretty obvious that it was colon cancer. However, Colon cancer is a carcinoma and only four carcinoma spread hematogenously. CRC isn't one of them. Why ISN'T the answer: tumor seeding of the abdominal cavity from the colonic tumor? Thank you! +3  
cheesetouch  @docinthehouse18 Not great insight, but I think the most classic case of seeding of abdomen is omental caking in ovarian cancer (but wiki also says assoc w colon and stomach). +  


submitted by ergogenic22(321),
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AINPQ is a oticx mietartenedi si rdeofm by in mlsal atmnuso by membsoital of teian.cnahepom eeilpDnot fo htcpiae oahlgniettu tssore yb QIANP edals ot acetu PAPA yxctioti adn ucate lrvie nijyr.u

cassdawg  Also relevant to the question: the CYP450 pathway is what turns acetaminophen into NAPQI, and chronic alcohol abuse is one of the inducers for the CYP pathway so it increases NAPQI production. Chronic alcohol abuse itself also depletes glutathione, increasing propensity for toxicity when acetaminophen is introduced. +  
specialist_jello  my probably stupid thought process was : treatment of acetaminophen toxicity is N acetyl cystine which regenerates gluathione. so toxicity will be coz of dec glutathione. +12  
i_hate_it_here  Real talk, can this site even charge for the contributions made by other people?? +1  
cheesetouch  FA18 470 & 243 +2  


submitted by andro(189),

Note: IL-12 receptor deficiency, or a defect in the Interferon Gamma receptor
Think Disseminated Mycobacterial and Fungal Infections . Also salmonella *

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). +2  
cheesetouch  FA2018 P 116 under il-12 receptor deficiency +2  
cheesetouch  Also on FA18 p 102 related to Th1 response +  


submitted by andro(189),

Patient with Primary Hypothyroidism (problem with the gland itself ) treated with T3

  • In normal physiology T4 is converted to T3 and less commonly ( rT3) . As such most of the T3 in the body is derived from the peripheral deiodination of T4 to T3
  • Also note that TSH secretion by anterior pituitary is under negative feedback control by both Free T3 and T4

So what happens when we give our Patient T3.
- firstly , we inhibit secretion of TSH from the pituitary gland . ( TSH decreases ).

This means less stimulation of the Thyroid and less hormone production . The Throid hormone it primarily makes and releases is T4 , ( and so T4 decreases ) . Naturally you would also expect a decrease in T3 but patient is taking exogenous T3( and so T3 increases )

schep  I messed this up because I know treatment of primary hypothyroidism is usually with levothyroxine (T4). I totally skimmed the part where we are told she is being treated with T3 +1  
jdc_md  ^nbme is asshoe! +1  
topgunber  side note thyroglobulin would also be low and is asked on uworld +2  
cheesetouch  Thyroxine = T4 +1  


submitted by bingcentipede(260),

The patient is presenting with hydronephrosis and a UTI. Remember, patients are prone to UTIs when urine is stagnant, so if there's an obstruction, there's an increased chance of UTI.

Being that it's a boy, there's a chance this is a posterior urethral valve that is obstructing the ureter.

cheesetouch  posterior urethral valve obstructs the ureTHRA, so the bladder would be effected (dilated, thick walled) and I feel like both ureTERs would be blocked. FA18 563. I think he's a bit too old, but hard to know. +2  
kbizzitt  Yea posterior urethral valve is typically picked up prenatally on ultrasound. The other finding would be oligohydramnios, so Potter sequence would likely be involved. FA20 579 +  


What you can see is

1.Hyperkeratosis (thickened stratum corneum) 2.Parakeratosis (you can see the nuclei very clearly in the stratum corneum) 3.Dysplasia (notice keratinocytes hyperchromatic and large nuclei go up almost all the way to the top. This isnt so in normal skin)

all this fits actinic keratosis

cassdawg  Actinic keratosis is FA2020 p482 if anyone needs it! +4  
baja_blast  FA2019 p. 472 +1  
cheesetouch  Sweet name @osler_weber_rendu #represent #cureHHT +  


First aid 2020 pg 511-- brain lesion in the subthalamic nucleus = contralateral hemiballismus

cheesetouch  also: Caudate atrophy -> Huntington Disease [causes cognitive issues FA18 p 484 vs putamen has motor role] Dentate nucleus is the most lateral deep nucleus involved in cerebellar output (FA18 p 483) +  


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irA adn flidu = rexapmtdoou.rhhoyn fI taht dfliu is dbloo p(/s tb,bgain)s ’sti a mhpenh.roxeutaomo cLka fo nmedsaatiil shift idsceanti that sti’ otn redun .isonent

d_holles  @benwhite_dotcom how can it not be under tension if air is entering the pleural cavity? +1  
nwinkelmann  Because the stab wound isn't functioning like a flap, meaning the air can escape. The reason a tension pneumothorax occurs is because the wound acts as a flap, where on inspiration it is open and air enters, but on expiration is closes and traps the air. +10  
groovygrinch  Also if there was tension, there would be a mediastinal shift. +11  
t123  Also the gastric bubble is elevated, actually suggesting lower pressure. Mediastinum shifts require more pressure, but the gastric bubble confirms it. +1  
myoclonictonicbionic  I was overthinking and thought they're implying that the stomach bubble is the air-food level that was seen on the Xray. +3  
cheesetouch  umm air-fluid*^ lol +1  


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TPT sha a cilascs e:tnpad hoproagctiancimi oclytmihe anma,ei totchomrbi ruaprp,u refve, ralen erfaul,i ignoroucle btoiaeamsinlr .()MAS hWeenrev uyo ees a ntsiueoq ehwre het nttpiea nsddeuly sah a lot igngo no, crsednoi TT.P

mgemge  Why is TSS wrong? +1  
aejinkim  @mgemge: the patient's BP is still up there, and for me, she doesn't have a crazy fever that i associated with when i think of TSS +  
cheesetouch  also TSS they would have to give you tampon use or nasal packing left in for a day. And it wouldn't cause schistocytes. +  
beltorres23  TTP pentad FAT RN: Fever, Anemia, Thrombocytopenia, Renal, Neuro symptoms +  
aakb  The big hint for me was schistocyte formation +  


submitted by lpp06(30),

I think this is actually just a complication of a Meckel's Diverticulum - Acute Meckel's Diverticulitis - which would be consistent with his presentation of acute abdomen + tarry black stools + CT/gross findings. It can be described as a mimic of appendicitis (as seen here).

I think if they wanted us to think this was Crohn's + Meckel they would have given us a more classical Crohn's presentation (skip lesions, insidious onset, non bloody stool)

cheesetouch  2 by 2xm bulge is a hint for meckels too (FA 'rule of 2's) +  
topgunber  Antimesenteric border is a big sign of meckels because its a true diverticulum +  


submitted by focus(28),

"The drainage pathways are as follows: (a) upper rectum: through the superior rectal nodes to the inferior mesenteric nodes, (b) lower rectum: from the lower rectum through the middle rectal nodes to the internal iliac nodes, and (c) anal canal: through the mesorectal (also known as inferior rectal) nodes to the inguinal and femoral nodes."

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4664281/

armageddon_oh  FA 2020: pg.366 USMLE loves them hemorrhoids. +  
cheesetouch  fa2018 p360 +  


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The orraw si ioingntp ot a uheoplintr ebluitdo(ml un)s:cuel anmi itfrehg of het meiumn sytsme in aecut aofmmtanliin nda tcrlbaeai nniioetfc chsu( sa iponasiatr )imuneopn.a a5C is a catthecicmo trofca orf .sPNM

ibestalkinyo  Other chemotactic factors include IL-8 and LTB4 +5  
j123  Note: C5a is a chemotactic factor for many immune cells in addition to neutrophils. Also, C3a is a chemotactic factor for just eosinophils and basophils (not neutrophils) +1  
cheesetouch  Q. What's so sexy about C5a? A. It's like Chanel No. 5 for neutrophils: they smell it and come running. +5  


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ilSpttngi is na rtmamiue eefsnde heincmams entof eemodply yb iattenps wiht inrbeedrlo eiarsopnylt dseoi.drr Wneh gnpslt,iit a esponr filas ot ees rotehs as ebacalp of vgnaih thbo piivetso dna tegavien ;qaetiisul at any gveni te,im i’ts lla ro g.ntnohi

d_holles  Got this one wrong -- thought it was acting out. +1  
cheesetouch  FA 2018 p539 the 'nurses are cold, doctors are friendly' example is what first aid uses too haha +  


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ihsT ntsuioqe is isgank rfo eth usvalcar lspupy of teh yrhiorpaadt a.ndsgl Ttha wduol be teh fnioeirr yodtrih areiet,sr ihwhc arise from het arotivhycrcel ktun.r

weenathon  I originally chose vein because I was thinking maybe the hormone release couldn't be carried to the body anymore, but looking back the working of "moderate hemorrhaging" and vessels requiring ligation is what implies it's an artery. Just throwing that out there in case you thought like I did. +4  
cheesetouch  if you were clueless like me (well I knew artery but..), picking one with 'thyro' in the name when discussing a thyroid surgery is a good guess :) +6  
cbreland  I'm really out here picking one of the answers with vein +  


submitted by em_goldman(24),
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bautmiRxi tC(i-aDn 0)2 is yrnelurtc eigrongnud itsrla for A.S My pessra ngoilggo ujst won wshso ahtt xamribuit bbplyroa ylon sah a drtoemea fee,cft os bplroayb ilcdsonene- to ntaaFN-iT hyt.eapr .bayblorP

Sfea to say rfo brsdoa ttah A:S FaTN ;> C20D

cheesetouch  FA 2018 - rituximab p 430 -- - use for Nonhodgkins lymphoma, CLL, ITP, Rheumatoid arthritis TNF-a inhibitors - p 472: 1) etanercept for Ra, psoriasis, ankylosing spondylitis. 2) infliximab and other mAB for IBD, RA, AS, psoriasis +1  


submitted by pelparente(21),

I believe this is rotavirus which is a common cause of fatal diarrhea in children. I think "wheel-like shape" is technically a buzz word for rotavirus, but I didn't know that. Yes, there is a vaccine, but it requires 2-3 shots giving within a month starting after 6 weeks of age so maybe this child isn't completely immune yet. Once you get to rotavirus you just need to know the rest and I linked the video below on how I remember all the viruses.

https://www.youtube.com/watch?v=Df_qAFF58Ec

cheesetouch  Rotavirus is the only dsRNA virus and is important/unique from that. +2  
overa  the vaccine is orally administrated +  


submitted by match95(48),
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niuQotes wsa ictkry -- eedn to oolk aet FEALOT llsve.e Bhto 21B feieidccny and faleto cedfyienci lwil ceaus an ecrinaes in ote.nosyemihc nylO B12 eneicfdyic lliw csuae an sncieear ni TBOH cnlmleaymthoi daic NAD ycmtnieeh.oso

cheesetouch  B12 deficiency 'BOTH be high' (and neuro sx) +  


This lady had preterm premature rupture of membranes. She had a genital tract infection, which is a risk factor for PPROM.

From Uptodate: Many of the microorganisms that colonize the lower genital tract have the capacity to produce phospholipases, which can stimulate the production of prostaglandins and thereby lead to the onset of uterine contractions. In addition, the host's immune response to bacterial invasion of the endocervix and/or fetal membranes leads to the production of multiple inflammatory mediators that can cause localized weakening of the fetal membranes and result in PPROM.

alimd  did you pay fucking $30? +1  
cheesetouch  some institutions give students UpToDate access +3  
cbreland  I knew that misoprostol (PGE1) can be used for abortions by forcing uterine contractions, so I figured the answer had something to do with prostaglandins +5  
rthavranek  I knew prostaglandins increased uterine contraction, but I also thought PGE2 caused cervical ripening and since there was a closed cervix, I eliminated that choice. I had no idea what was going on so I just picked oxytocin since that would increase uterine tone without dilation, though my reasoning seems to be incorrect +2  
utap2001  Great, the above message deserve $30. +  
notyasupreme  I think also it said that the fetus releases oxytocin and steroids, which I guess is stupid wording that makes it not right. Anyways, fuck the curve on NBME 18 :) +3  
okokok1  if anyone didn't know what "PPROM" stood for it is: Preterm Premature Rupture Of Membranes" +2  
aakb  I was between the prostaglandin answer and stressed fetal production and release of oxytocin and the reason I didn't pick oxytocin was if the cervical os is closed (membranes ruptured 32 hrs ago and contractions been going on for 12) and there's no effacement, it didn't seem like that baby actually wanted to come out so I thought that's not what's happening here. Plus mom has a fever so inflamed maternal decidua seemed to fit. +  
helppls  If there was an increase in Pgs why did she not have a ripened cervix? +  


submitted by tissue creep(113),
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ildM jieuadcn hiwt nedrsiaec jendgcuotuna ni na drole elfwol is sdedecear tnnyusegscDuf-eUrolPalrar ct.vityai uaylarPtrilc in xttcoen fo rsstes p)(tenapmdeyoc

pg32  Went with hepatitis because of his recent surgery. Seen problems like this before where recent surgery means they were given inhaled anesthetic that can cause hepatotoxicity/hepatitis. That, along with the elevated AST/ALT and unconjugated bilirubinemia (signifying liver losing its ability to conjugate bilirubin due to inflammation) made me pick hepatitis. Why is that wrong? +  
suckitnbme  @pg32 AST/ALT are only slightly elevated. The patient also is not particularly symptomatic. He's really not that sick. Hepatoxicity is also most associated with halothane which is no longer used in the US. It would be a different story if the patient had surgery done in a different country (as is common in Uworld questions on this) +5  
mumenrider4ever  I don't know why NBME uses ALT/AST reference ranges from 8-20 u/L when the reference ranges for uworld are 8-40 u/L. So maybe his liver enzymes aren't really elevated since they're below 40 +4  
cheesetouch  Can someone refute 'surgical trauma'? +  
cancelstep  Appendix is pretty far anatomically from the bile ducts. Also damage to bile ducts should cause direct hyperbilirubinemia since there's no problem with conjugation versus Gilbert syndrome which causes impairment of UGT +4  


submitted by cassdawg(1165),

In hypothesis testing, the alpha value is the probability of making a Type I error. This is the type of error mentioned in the question.

  • Type I error - you find a difference when a difference doens't really exist.
    • One way of remembering this is that this is what scientists "want" to make: they want to find a significant difference in their data, thus it is the "first mistake" they'd make.
    • Alpha is the probability you are willing to accept that you could have made a type I error (i.e. an alpha value of 0.05 means there is a 5% probability you could make a type I error and reject the null hypothesis when you should not)

  • Type II error - you do not find a difference when you should have because a true difference really exists
    • Beta is the probability that you make a type II error
    • Power is equal to (1 - beta)
    • Power can be increased by increasing sample size, and thus with a larger sample you have a lower probability of making a Type II error
    • Power can also be increased by increasing expected effect size or increasing precision. It is interesting to note accuracy has no effect on power.

FA2020 p263

cheesetouch  FA2018 p258 +  


submitted by cassdawg(1165),

I don't like this question for many reasons, but basically he has sarcoidosis (noncaseating granulomas with no pathogen found on biopsy) which according to First Aid is more common in African-American females. Since he is African-American that is his risk factor (FA2020 p676).

cheesetouch  FA2018 p658 +  
i_hate_it_here  Questions like this let me know that the ideals of racism have never left the medical system. Ok, so he's "African-American", is he of actual African descent? Is sarcoidosis just increased in american found black people, or is it black people of African descent, what about Jamaican? Afro-Latino, Europeans?? I hate that they teach us things like this and we're suppose to take it at face value. +1  
kaf  agree...medicine is full of racism, sexism and so on. Some meds work differently and diseases present differently etc...for ex., ACE inhibs in AA vs white...or MI presentation in women vs men. +  


submitted by baja_blast(113),

Cocaine use in pregnancy is associated with low birth weight, premature membrane rupture and abruptio placentae. Click here for more.

FA 2019 p. 600 gives a list of drug effects during pregnancy.

cheesetouch  teratogens FA2018 p596 +1  


submitted by cassdawg(1165),

This girl has an ectopic thyroid that has remained attached to the tongue by thyroglossal duct. The mass can be identified as an ectopic thyroid rather than a thyroglossal duct cyst due to the uptake to Tc99 pertectnetate. Thus, a biopsy would show thyroid follicles. (FA2020 p326)

cheesetouch  FA2018 P320 +1  
cheesetouch  CONTRAST - branchial cleft cyst in lateral neck from persistent cervical sinus would not move w/ swallowing or tongue protrusion +1  


submitted by cassdawg(1165),

This girl has an ectopic thyroid that has remained attached to the tongue by thyroglossal duct. The mass can be identified as an ectopic thyroid rather than a thyroglossal duct cyst due to the uptake to Tc99 pertectnetate. Thus, a biopsy would show thyroid follicles. (FA2020 p326)

cheesetouch  FA2018 P320 +1  
cheesetouch  CONTRAST - branchial cleft cyst in lateral neck from persistent cervical sinus would not move w/ swallowing or tongue protrusion +1  


submitted by cassdawg(1165),

The ductus arteriosus is kept patent by prostaglandins (which is why the baby is started on a prostaglandin drip id we need to keep the ductus patent in some hypoxic congenital heart diseases).

Thus, to close the PDA, prostaglandins are decreased. cyclooxygenase inhibition (COX) is one way of decreasing prostaglandins and is the physiologic way of closing the ductus as well as how we close it if necessary (to close a PDA you give a baby NSAIDs, FA2020 p486).

cheesetouch  NSAIDs p471 FA2018 +2  


submitted by cheesetouch(140),

Frothy YELLOW GREEN DISCHARGE, motile organism with flagella -> dx of trichomonas vaginalis, treatment is metronidazole for patient and partner. FA2018 P158.

Trichomonas vaginalis is an STI with foul smelling green discharge, trophozoites on wet mount.

cheesetouch  intravaginal miconazole is the treatment of candida vaginitis (white cottage cheese discharge) +  


submitted by hungrybox(1044),

These are really the only two that should be on your differential for a diaphragmatic hernia:

A: Abnormal relation of the cardia to the lower end of the diaphragm | Sliding hiatal hernia

B: Protrusion of the fundus into the chest above the level of T10 | Correct! This describes a paraesophageal hernia.

different hernias

parts of stomach

cheesetouch  FA2018 P364 +  


submitted by cassdawg(1165),

My take on this question is that he is about to be diagnosed with advanced stage pancreatic cancer, which has a high mortality rate. On its own, pancreatic adenocarcinoma is not associated with any of the psychological disorders. However, a diagnosis of a terminal condition or advanced cancer of any kind that would require aggressive treatment with poor prognosis would be associated with major depression. Thus, he is at most risk of major depressive disorder.

cheesetouch  Study break journal article about depressive symptoms before pancreatic cancer diagnosis - https://journals.lww.com/pancreasjournal/FullText/2018/04000/Early_Detection_of_Pancreatic_Cancer__The_Role_of.1.aspx +5  
trazobone  Did anyone else think that the mass would considerably extend into the terminal ileum and then cause a deficiency of B12 absorption, thus leading to memory impairment LOL +1  


submitted by cassdawg(1165),

This patient likely has Gilbert syndrome (FA2020 p394).

This is because his hyperbilirubinemia occurs during periods of stress and is relatively benign. Gilbert's syndrome has elevated unconjugated bilirubin because there is a mild deficiency in UDP-glucuronyltransferase conjugation. Thus, the cause is decreased conjugation of bilirubin.

cheesetouch  FA2018 P387-388 +  


submitted by cassdawg(1165),

Based on the history (consumption of large amounts of alcohol and elevated serum amylase/lipase with hypocalcemia), this man likely has acute pancreatitis (FA2020 p397). One of the major complications is autodigestion of tissues, such as what is seen in the image.

cheesetouch  FA2018 P391 +  
epiglotitties  Can anyone explain/describe the image? I got it right based on the info from the question but would like to know anyways just for future reference +1  
randi  FA2019 391 It's also not alcoholic hepatitis because this "requires sustained, long term consumption" of alcohol and this patient consumption over the last few days. FA2019 395 +  
whk123  Morphology to acute pancreatitis +1  
hecticsurreyguy  @epiglotitties this is purely a stab on my part but... I'm seeing variation in size and consistency of the adipocytes in the image, along with vesicular changes in several of the adipocytes in the bottom right hand corner of the figure. These would point towards lipolytic reaction being undergone in these adipocytes. +  


submitted by cassdawg(1165),

The description points to pancreatic insufficiency due to steatorrhea (fat in the stool, likely due to insufficiency of pancreatic lipase) and muscle fiber in the stool (which points to incomplete protein digestion, likely due to insufficiency of pancreatic proteases).

Further, he has no deficiency in carbohydrate absorption as evidenced by the D-xylose test (which indicates an intact mucosa for absorption and does not require digestive enzymes, FA2020 p373); and he has no abnormalities on biopsy of the intestine.

Thus, the primary issue is pancreatic insufficiency and supplementation of pancreatic enzymes is most helpful.

cheesetouch  FA2018 P375 +1  


submitted by cassdawg(1165),

TL;DR: Even with Type I or II renal tubular acidosis the ammoniagenesis from glutamine is not impaired and thus is the main source of ammonia.

Here is my take: Based on her history and measured plasma values, this girl likely has one of the "low potassium" renal tubular acidoses, either Type I or Type II (see this chart for reasoning based on measured values or this image for fun colorful renal tubular acidosis and FA2020 p593)

Then, we are told that she has a defect in "ammoniagenesis". In the renal tubules, ammonia is generated in two primary ways: via direct conversion of glutamine to ammonia in the proximal tubule which is then secreted into the tubule, or by NH3 combining with with H+ in the collecting tubules (which I guess they are considering a separate ammoniagenesis pathway even though its all kinda related?). See this diagram or this diagram

Assuming our girl has Type I renal tubular acidosis, there will be decreased availability of hydrogen ions in the renal tubules to combine with NH3. Thus, the primary source of ammonia production in this patient will be glutamine (which is the major source of ammoniagenesis in a normal person anyways).

Further reasoning - Type I is impaired secretion of hydrogen ions into the lumen, so there will be less hydrogen ions available. She likely has type I because this is primarily treated with potassium citrate (both to buffer and to prevent renal stones which are a common complication). Even if she had Type II the increased excretion of bicarb would also buffer more H+ leaving less for ammoniagenesis in the NH3/H+ combination fashion.

Contrarily, Type 4 renal tubular acidosis (hyperkalemic) results in decreased synthesis of ammonia in the proximal tubules, which we know she does not have because of her low potassium.

cheesetouch  Cassie you're a god. Simple/stupid approach to make a good guess - if she cannot make ammonia in the kidney, main ammonia source probably from an exogenous form like amino acids -> Glutamine! +3  
pakimd  thank you @cassdawg, you're amazing! +  


submitted by ergogenic22(321),
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CTL srcdeeade esstusgg crtvteriies s.asieed uRaetcilr ptatenr essgtsgu nyolapmur ibosfrsi

cheesetouch  fa2018 p657 +  
whk123  So after seeing clubbing of fingers we have two D/D's in our mind 1)Bronchiectasis (a type of COPD in which TLC increases your lungs expand due to obstruction air can't go out from lungs so air keeps on expanding lungs) 2)Idiopathic pulmonary fibrosis why IPF is a ans here because in q stem TLC is decreased and the coarse reticular pattern (honeycomb appearance) is also a giveaway. +  


submitted by cassdawg(1165),

This woman has pulmonary hypertension, likely pulmonary arterial hypertension characterized by increased pulmonary artery pressure with a normal pulmonary capillary wedge pressure (remember pulmonary capillary wedge pressure is associated with left atrial pressure). PAH endothelial dysfunction causes an imbalance in vasoconstrictors (such as endothelin) and vasodilators (NO and prostacyclin). [FA2020 p679]

BosENtan, used to treat PAH, is an ENdothelin antagonist (FA2020 p686)

cheesetouch  FA0281 p667 +  
scoresloth  I thought it was a prostacyclin analog. +  


submitted by cassdawg(1165),

He has alpha-1 antitrypsin deficiency which is causing panacinar emphysema and liver damage. This is the major disease to think of when you have a young-ish patient who presents with liver and lung issues. (FA2020 p392)

From the stem: hyperinflation combined with decreased diffusion capacity and decreased FEV1 points toward emphysematous change; lower lobe predominance is seen in panacinar emphysema; hepatomegaly pointing to liver involvement

NOTE: diffuse idiopathic interstitial fibrosis would cause a decreased diffusion capacity, but this is a restrictive lung disease which would not have hyperinflation but instead decreased lung volume

cheesetouch  FA2018 p386 +1  


submitted by fruitkebabs(20),

This is Pierre Robin sequence, which presents with micrognathia, glossoptosis, cleft palate, and airway obstruction.

It is one of the First Arch syndromes, and the major tip off in the stem would be the mandibular cleft since the mandible is derived from 1st pharyngeal arch.

cheesetouch  fa2018 p602 +  
cheesetouch  Glossoptosis is a medical condition and abnormality which involves the downward displacement or retraction of the tongue. +1  
i_hate_it_here  I hate your name lmao +  
raulirios  FA2020 p620 +  


submitted by fruitkebabs(20),

This is Pierre Robin sequence, which presents with micrognathia, glossoptosis, cleft palate, and airway obstruction.

It is one of the First Arch syndromes, and the major tip off in the stem would be the mandibular cleft since the mandible is derived from 1st pharyngeal arch.

cheesetouch  fa2018 p602 +  
cheesetouch  Glossoptosis is a medical condition and abnormality which involves the downward displacement or retraction of the tongue. +1  
i_hate_it_here  I hate your name lmao +  
raulirios  FA2020 p620 +  


submitted by cheesetouch(140),

Left dominant circulation - posterior descending artery (PDA) which supplies AV node etc is coming from the *left circumflex. Prompt says it is blocked. To get to there, the correct anatomical pathway is Left coronary artery, circumflex artery, posterior interventricular (PDA).

This can be reasoned by process of elimination too. 1- Given the Left dominant circulation, we can eliminate pathways beginning at the right coronary. 2- To get blockage at posterior of heart, we will NOT use anterior interventricular artery, so you can eliminate the 2 options listing those. 3 - The circumflex artery gives rise to the PDA, but is not the final artery in our path to the blockage (so can eliminate another two). This should give you the correct answer.

cheesetouch  FA2018 P277 heart anatomy drawing +  


submitted by cassdawg(1165),

Lentigo maligna is a type of melanoma (FA2020 p484), hence why it is important the lesion is brown/black with irregular borders and enlarging (all hallmarks of melanoma). The biopsy description also fits lentigo maligna, but even if you are not a pathologist the description that fits cancer and and "atypical melanocytes" should point you to lentigo maligna.

  • Acanthosis nigricans is thickening (acanthosis means epidermal hyperplasia) and darkening of skin in folds and creases associated with insulin resistance
  • Actinic keratosis is a premalignant lesion that is a small, rough, erethematous or brownish papule/plaque
  • Compound nevus is a type of mole that is slightly elevated, brown or light brown, and has regular borders. It is not fast-growing.
  • Sebhorreic keratosis are "stuck-on" flat, greasy, pigmented squamous epithelial proliferation of immature keratinocytes with keratin-filled cysts. Rapid onset of multiple indicates possible GI malignancy.

FA2020 p482, 477 and 484

cheesetouch  fa2018 p 469 melanoma +1  
randi  FA2019 p473 +  


submitted by ergogenic22(321),
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He ash a dwon adn tuo iuplp, cdeusa by CN III spay.l Hsi gzae si ued ot esdpuonpo caonit of eth eralalt reusct and rsuroipe ulbqieo; psiots eud to vontaedneir fo tleravo aeelpbpar sissr.eiupo

heT oyln jiryun iedslt htta luodc uaces a NC III ayspl is ermynusa of eht CAP censpirgmos het lmcroruooat .seucunl

cheesetouch  Compression of superior cervical ganglion -> Horner's syndrome -> ptosis, miosis, anhidrosis, would NOT have dilated pupil. +2  
jmd2020  Aneurysm of the PCA would compress the oculomotor NERVE, not the nucleus (just fyi) +2  
trazobone  I appreciate u cheesetouch +  


submitted by ergogenic22(321),
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alCssci riptecu fro nDenehcu sucaulrm ptyyodsrh. chiwh si deu ot ddleete tdopynsihr irtnep.o

romF FA: tnp"rDhyiso lhsep hracno mlceus berfis, rimirlapy in tekllesa nda iaraccd .ulsmce tI encnscto het allcerrnlitua elsnetkotyco (aintc) ot teh bentnsareamrm osieptrn -α adn syrgcy-na,βotld hwcih ear ntdeeccno ot teh arelcaltuerxl artxim C)ME"(

cheesetouch  fa2018 p61 +1  


submitted by cassdawg(1165),

Here is a summary of derivatives of neural crest cells. Also FA2020 p613 for embryologic derivatives [MOTEL PASSES - Melanocytes, Odontoblasts, Tracheal cartilage, Enterochromaffin cells, Leptomeninges (arachnoid, pia), PNS ganglia (cranial, dorsal root, autonomic), Adrenal medulla, Schwann cells, Spiral membrane (aorticopulmonary septum), Endocardial cushions (also derived partially from mesoderm), Skull bones]

cheesetouch  FA2018 P595 +1  


submitted by cassdawg(1165),

For gonadal drainage: (FA2020 p624)

  • Testes/ovaries drain to paraaortic lymph nodes
  • Body of uterus/cervix/superior bladder to external iliac
  • Prostate/corpus cavernosum, proximal vagina/cervix, and anus above pectinate to internal iliac
  • Distal vagina/vulva, scrotum, and anus below pectinate to superficial inguinal
  • Glans penis to deep inguinal

Basically, the superficial inguinal drains the skin below the umbilicus (except the popliteal area) and the other answers except the correct one are not associated with gonadal drainage

Lymph drainage FA2020 p97

cheesetouch  FA 2018 p606 - gonadal drainage +  


submitted by cassdawg(1165),

This indicidual has CATCH22 DiGeorge Syndrome, caused by failure in the development of the 3rd and 4th pharyngeal pouches (FA2020 p116). This is evidenced by the hypocalcemia (agenesis of parathyroids), facial deformities, and conotruncal abnormality (right sided aortic arch).

Big thing is being able to ensure you know it is pharyngeal POUCH not cleft or arch. Pharyngeal arch derivatives are on FA2020 p620. Pharyngeal pouch derivatives are p621. And pharyngeal cleft derivatives are p619. (Aortic arch derivatives are p619 as well, if you want to complete the circle)

Treacher-Collins is error in 1st and 2nd pharyngeal arch derivatives which can present with craniofacial abnormalities, zygomatic and mandibular hypoplasia, and hearing loss. Pierre Robin is similar and presents with micrognathia, glossoptosis, cleft palate, and airway obstruction. Neither of these would present with hypocalcemia.

cheesetouch  FA2018 P602-603 arches/pouches +  
cheesetouch  Arch vs pouch (my thoughts): Arches help build a structure and direct development of cartilage, muscles, nerves. Pouches are cavities or minor organs (middle ear cavity, eustachian tube, thymus, parathyroids). +7  


submitted by cassdawg(1165),

This indicidual has CATCH22 DiGeorge Syndrome, caused by failure in the development of the 3rd and 4th pharyngeal pouches (FA2020 p116). This is evidenced by the hypocalcemia (agenesis of parathyroids), facial deformities, and conotruncal abnormality (right sided aortic arch).

Big thing is being able to ensure you know it is pharyngeal POUCH not cleft or arch. Pharyngeal arch derivatives are on FA2020 p620. Pharyngeal pouch derivatives are p621. And pharyngeal cleft derivatives are p619. (Aortic arch derivatives are p619 as well, if you want to complete the circle)

Treacher-Collins is error in 1st and 2nd pharyngeal arch derivatives which can present with craniofacial abnormalities, zygomatic and mandibular hypoplasia, and hearing loss. Pierre Robin is similar and presents with micrognathia, glossoptosis, cleft palate, and airway obstruction. Neither of these would present with hypocalcemia.

cheesetouch  FA2018 P602-603 arches/pouches +  
cheesetouch  Arch vs pouch (my thoughts): Arches help build a structure and direct development of cartilage, muscles, nerves. Pouches are cavities or minor organs (middle ear cavity, eustachian tube, thymus, parathyroids). +7  


submitted by cassdawg(1165),

Based on the question stem and the autoanitbodies given (butterfly rash combined with anti-dsDNA/anti-Sm/antiphospholipid), this woman has classic lupus. SLE is associated with cytopenias, so thrombocytopenia is the best choice of the available answers. Thrombocytopenia is common in lupus (FA2020 p470)

  • HUS is associated with E.coli or Shigella infection and not Lupus. Lupus kidney disease is diffuse proliferative glomerulonephritis.
  • Macrocytic anemia is typically caused by B12 or folate deficiency and not associated with lupus. Lupus anemia is typically anemia of chronic disease, which is normocytic, or due to inadequate RBC production or iron deficiency, which is microcytic.
  • Multiple nucleated erythrocytes are found in leukemias when the RBCs are being "pushed" out of the bone marrow, or in diseases where the bone marrow is highly stressed. Lupus does not typically cause this.
  • I am not 100% sure why rouleax formation is wrong, because as far as I understand any condition that increases monoclonal Abs can cause rouleaux formation, but I am assuming it is just not as common/likely, hence thrombocytopenia which is very common is the better answer
cheesetouch  FA2018 P458 +1  
randi  FA2019 p462 +  


submitted by andro(189),

Myeloproliferative Disorders :

They are all associated with the JAK STAT mutation with the exception of CML which is associated with the fusion gene BCR:ABL ( from t(9;22 )-i.e philadelphia chromosome )

CML Tx : imatinib - BCR-ABL Tyrosine kinase inhibitor

TX of the myeloproliferative disorders - Ruxolitinib - Janus kinase inhibitor

cheesetouch  FA2018 P420-421 +  
shieldmaiden  FA2020 432-433 +  


So does someone know what is phase 0 for? It was an option... somathing like "let me see if i can study this thing?"

cheesetouch  via google - A Phase 0 study gives no data on safety or efficacy, being by definition a dose too low to cause any therapeutic effect. Drug development companies carry out Phase 0 studies to rank drug candidates in order to decide which has the best pharmacokinetic parameters in humans to take forward into further development. +  
boostcap23  Phase 0 is an extremely small dose (1% of normal) given to easily rule out any harmful effects. Basically used as a quick way to eliminate further trails/research on drugs that don't work. +1  


submitted by cassdawg(1165),

Bethanechol is a muscarinic cholinergic antagonist with no action on nicotinic ACh receptors. Bethanechol is commonly used to treat urinary retention by activating bladder smooth muscle via M3 Gq receptors that function by increasing phospholipase C conversion of PIP2 (phosphoinositide) to IP3 and DAG (FA2020 p240, p237, p238).

Wrong answers:

  • Atropine is a muscarinic antagonist which would non increase phosphoinositide turnover but decrease it (FA2020 p241)
  • Neostigmine is an indirect cholinergic agonist that works by inhibiting acetylcholinesterase that does work at the muscarinic synapse as well and is used for myasthenia gravis as well as postoperative ileus and urinary retention
  • Succinylcholine is a depolarizing muscarinic agonistnthat causes sustained depolarization and prevents contraction, used as a paralytic in anesthesia (FA2020 p551)
  • Trimethaphan is a drug that counteracts cholinergic transmission at the nicotinic receptors of the autonomic ganglia and therefore blocks both the sympathetic nervous system and the parasympathetic nervous system. It is used to treat hypertension
cheesetouch  FA2018 P236 +2  
jmd2020  Bethanechol is a muscarinic AGONIST, not antagonist (other it would further exacerbate BPH) +2  


submitted by andro(189),

A note to self : Creatine phosphate is a short term energy source in muscle . Acts by donating phosphate groups to regenerate ATP .

*Creatine is derived from Arginine and metabolised to Creatinine ( which is excreted by the kidneys )

cheesetouch  ATP on FA2018 p74 to annotate book +1  


submitted by cassdawg(1165),

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.

cheesetouch  FA2018 p157 too :) +  


submitted by cassdawg(1165),

Important aspects of volatile (gas) anesthetics: (FA2020 p549):

  • MAC (minimum alveolar concentration): essentially the ED50 for inhaled anesthetics, this is the minimum concentration of anesthetic that causes a response in 50% of patients
  • LOW MAC means HIGH potency - more potent drugs would have a lower minimum amount needed to be present in the alveoli in order to exert their effect.
  • LOW MAC is related to HIGH lipid solubility (higher oil/gas partition coefficient) - more lipid soluble agents tend to be more potent because of their increased ability to cross the BBB
  • MACs are additive (i.e. one gas at 1.5 MAC = two gases at 0.75 their respective MACs)
  • Blood/gas partition coefficient: an expression of solubility; anesthetics with a low blood gas partition coefficient have a rapid onset/offset
  • i.e. LESS plasma solubule anesthetic = FASTER onset/offset
  • This is because less plasma soluble agents will "fill up" their maximum amount in the blood reservoir quicker and thus are pushed down their concentration gradient into the brain quicker; i.e. they quickly saturate the blood and will move on to affecting the brain quicker
  • MAC and blood/gas partition coefficient also tend to be inversely related -- higher MAC = lower blood/gas partition coefficient and vice versa; thus many of the more potent anesthetics have a longer time for onset/offset
cheesetouch  FA2018 P532 +1  
randi  FA2019 p536 +  


submitted by andro(189),

Note: IL-12 receptor deficiency, or a defect in the Interferon Gamma receptor
Think Disseminated Mycobacterial and Fungal Infections . Also salmonella *

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). +2  
cheesetouch  FA2018 P 116 under il-12 receptor deficiency +2  
cheesetouch  Also on FA18 p 102 related to Th1 response +  


submitted by cassdawg(1165),

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

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


submitted by cassdawg(1165),

A cleft lip/palate with no associated anomalies has multifactorial etiology (FA2020 p621). There is no evidence of associated syndrome or inheritance, so it is multifactorial.

cheesetouch  FA2018 p603 +  
randi  FA2019 p607 +  
whoopthereitis  just fun stuff to add: Other diseases that can also be considered multifactorial are Spina Bifida, DM, CAD, HTN. Had this question somewhere else once. +  


submitted by fruitkebabs(20),

Oseltamivir and zanamivir are influenza neuraminidase inhibitors. Typically, neuraminidase allows influenza particles to bud off host cells. Without the functioning enzyme, the virion buds cannot detach from the host cell membrane.

cheesetouch  FA2018 P201 +1  


submitted by cassdawg(1165),

The proteasome degrades ubiquitin-tagged proteins into amino acids and releases ubiquitin for recycling.

See here for picture illustration of the process.

cheesetouch  FA2018 p48 +1  


submitted by cassdawg(1165),

Lipopolysaccharide, or LPS, is the primary endotoxin mediator of gram(-) sepsis leading to septic shock. This woman likely has sepsis from E. coli, a gram negative bacterium which produces LPS, based on her history indicating a UTI. E.coli are the most common cause of UTI. (FA2020 p133)

cheesetouch  FA2018 p145 +6  


submitted by cheesetouch(140),
1 tumor w/ met to liver is colon cancer Fa2018 p226
cheesetouch  sorry for a lazy answer folks! +5  
docinthehouse18  Yes it was pretty obvious that it was colon cancer. However, Colon cancer is a carcinoma and only four carcinoma spread hematogenously. CRC isn't one of them. Why ISN'T the answer: tumor seeding of the abdominal cavity from the colonic tumor? Thank you! +3  
cheesetouch  @docinthehouse18 Not great insight, but I think the most classic case of seeding of abdomen is omental caking in ovarian cancer (but wiki also says assoc w colon and stomach). +  


submitted by cassdawg(1165),

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.

cheesetouch  FA2018 P364 CDH +1  
randi  FA2019 364 Diaphragmatic Hernia +  


submitted by cassdawg(1165),

The image shown is one of asbestosis (asbestos bodies resemble dumbbell, as seen here and found FA2020 p677). Aside from the image, he also has the major risk factor of asbestosis of working in a shipyard. Asbestosis typically affects the lower lobes of the lungs (hence the bibasilar crepitant crackles) and carries the ability to cause reticulonodular pulmonary infiltrates / fibrosis.

Similar to the pathology behind silicosis fibrosis, alveolar macrophages respond to aesbestos and release fibrogenic factors.

Alveolar macrophages phagocytize foreign materials, release cytokines and alveolar proteases.

Type I pneumocytes make up the alveolar lining, and Type II pneumocytes generate surfactant and can proliferate into Type I pneumocytes in response to alveolar damage. Kulchitsky cells are cells of origin of small cell lung cancer. Clara cells (now called club cells) are nonciliated bronchiolar exocrine cells that secrete a component of surfactant, degrade toxins, and act as reserve cells.

flapjacks  A barbell, really. +1  
cheesetouch  FA2018 P659 +8  
jer040512  eh... more like a shake weight. +2  


submitted by cassdawg(1165),

Thiazide diuretics can cause hypokalemia (FA2020 p609).

cheesetouch  FA2018 P 591 +1  


submitted by bingcentipede(260),

The classic triad of a renal cell carcinoma is: 1) hematuria; 2) flank pain; and 3) a palpable flank mass. The classic RCC comes from a VHL mutation. No VHL means you can't inhibit HIF (hypoxia inducible factor). This leads to uncontrolled activation of VEGF, leading to the hypervascular mass.

cheesetouch  FA2018 P583 +2  


submitted by cassdawg(1165),

Epstein-Barr virus is associated with lymphomas (endemic Burkitt Lymphoma, Hodgkin lymphoma, CNS B-cell lymphoma), nasopharyngeal carcinoma, and lymphoproliferative disease in transplant patients. (FA2020 p164)

Here is a chart of virus-associated cancers and their viruses. Also found FA2020 p226.

  • CMV is not associated with cancer but is associated with AIDS retinitis and esophagitis.
  • Hepatitis B is associated with hepatocellular carcinoma.
  • HHV-8 is associated with Kaposi sarcoma in AIDS patients (an endothelial neoplasm, FA2020 p478)
  • HTLV-1 (human T-CELL...) is associated with adult T-cell leukemia
cheesetouch  FA2018 P165 +1  
cheesetouch  Additionally, HTLV is a ss+RNA Retrovirus and prompt mentions DNA probe. All other viruses are DNA genomes. +  


submitted by cassdawg(1165),

Epstein-Barr virus is associated with lymphomas (endemic Burkitt Lymphoma, Hodgkin lymphoma, CNS B-cell lymphoma), nasopharyngeal carcinoma, and lymphoproliferative disease in transplant patients. (FA2020 p164)

Here is a chart of virus-associated cancers and their viruses. Also found FA2020 p226.

  • CMV is not associated with cancer but is associated with AIDS retinitis and esophagitis.
  • Hepatitis B is associated with hepatocellular carcinoma.
  • HHV-8 is associated with Kaposi sarcoma in AIDS patients (an endothelial neoplasm, FA2020 p478)
  • HTLV-1 (human T-CELL...) is associated with adult T-cell leukemia
cheesetouch  FA2018 P165 +1  
cheesetouch  Additionally, HTLV is a ss+RNA Retrovirus and prompt mentions DNA probe. All other viruses are DNA genomes. +  


submitted by cassdawg(1165),

Loratadine is a second generation antihistamine and thus would be preferred in this patient as it does not cause sedation. [FA2020 p686]

Since he works operating heavy machinery, it would be preferred to put him on a second generation antihistamine. Bropheniramine, hydroxyzine, and diphenhydramine are first generation antihistamines which cause sedation.

Ranitidine is a histamine H2 blocker used to decrease secretion by parietal cells in peptic ulcer disease, gastritis, and gastric reflux [FA2020 p399]

cheesetouch  FA2018 P667 +  


submitted by lfcdave182(32),

Pg 391, FA 2020

  • Alcoholic hepatitis: Swollen and necrotic hepatocytes with neutrophilic infiltration; Mallory Bodies (Intracytoplasmic eosinophilic inclusions of damaged keratin filaments)
cheesetouch  FA2018 P385 +4  
randi  FA2019 p.385 +1  


submitted by cassdawg(1165),

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.

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  


submitted by cassdawg(1165),

Spironolactone has a special use in hepatic ascites (FA2020 p609).

Spironolactone is the drug of choice for initial treatment of ascites due to cirrhosis

cheesetouch  FA2018 P591 +  
mittelschmerz  In portal HTN, the splanchnic vasodilation results in a drop in systemic BP and renal hypoperfusion. That leads to RAAS activation that increases SBP enough to maintain renal perfusion, but the aldosterone-mediated Na/H2O retention leads to edematous states (ascites here). Treating with spironolactone allows you to treat the the fluid component without disrupting the vasoconstrictive effects of AngII that is the only thing maintaining renal perfusion, which is why spironolactone is correct here, but also why prescribing an ACEi or ARB in a hepatic patient like this is v v bad. +9  
nbmesucks  I just took it as this guy is on a loop diuretic so he's gonna lose his potassium. So to minimize this we give a potassium sparing diuretic. +3  


submitted by cassdawg(1165),

This is one of the main consequences of liver failure. [FA2020 p389]

The proposed mechanism is an imbalance in free testosterone and estrogen caused by defect in sex hormone binding globulin (more free estrogen = gynecomastia).

cheesetouch  FA2018 P383 see image in 'cirrhosis and portal hypertension' +  


The prednisone will induce T cell apoptosis (FA2020 pg 120)

cheesetouch  FA2018 p120 +  


submitted by cassdawg(1165),

This is normal menopause (FA2020 p636). Average age of onset is 51 years (our woman is 52). Hot flashes are a common symptom.

In menopause, the ovaries stop secreting estrogen (17beta-estradiol is an estrogen) due to a decline in the number of ovarian follicles with age. FSH is increased because the feedback inhibition is removed. The source of estrogen after menopause becomes peripheral conversion of androgens.

peteandplop  FA2019 p622 +2  
cheesetouch  FA2018 P617 +  
sexymexican888  Estradiol (ovary) > estrone (peripheral) > estriol (placenta) The way I remember the strength "diol" kind of sounds like god in spanish "dios" so its the strongest, then the "throne" for "trone" and then triol the "trio" like god, holy spirit and jesus lol im not super religious but this helped me remember the order! and triol is placenta -> jesus was a baby haha +  


submitted by cassdawg(1165),

Ligation of the internal iliac artery is used to stop postpartum uterine bleeding while preserving fertility as the ovarian arteries provide collateral circulation (FA2020 p640).

Here is an image showing the uterine artery coming off the internal iliac with the ovarian artery collateral.

Other answers:

  • The external iliac gives rise to the femoral artery, inferior epigastric artery, and the deep circumflex iliac artery
  • The internal pudendal artery supplies the external genetalia and perineum via arteries such as the inferior rectal artery (anal canal BELOW the pectinate line), perineal artery, and ldorsal/deep arteries of the clitoris or dorsal/deep arteries of the penis
  • The median sacral artery is small and supplies the coccyx/sacrum/lumbar vertebrae
  • The obturator artery is a branch of the internal iliac which gives off the pubic branch (supplies pelvic muscles) and acetabular branch (supplies head of the femur)
cheesetouch  fa2018 p624 +3  


submitted by cassdawg(1165),

This is feedback inhibition of the RAAS (renin-angiotensin-aldosterone system) axis. Increased aldosterone will feedback and inhibit renin secretion of the kidney. (FA2020 p588)

flapjacks  Increased serum sodium concentration is not specific enough to support the diagnosis +7  
cheesetouch  Fa2018 p332: Hyperaldosteronism - primary hyperaldosteronism seen with adrenal adenoma (Conn syndrome). High aldosterone, low renin. Causes resistant hypertension. +3  
mark0polo  Serum sodium concentration wouldn't actually change because of the aldosterone escape mechanism in primary hyperaldosteronism +8  
i_hate_it_here  <- +1  


submitted by cassdawg(1165),

This woman likely has endometriosis, characterized by cyclic pelvic pain, bleeding, and associated with infertility (FA2020 p648). It is associated with "chocolate cysts" on the ovaries. Proliferative endometrial tissue would be found on biopsy

Endometriosis scar tissue/adhesions can cause the uterus to stick in a backwards position (retroverted) according to https://www.healthline.com/health/womens-health/tilted-uterus

Polycystic ovarian syndrome is associated with obesity would also likely have symptoms of hisutism and acne as well as infertility. It also presents with amenorrhea or oligomenorrhea. [FA2020 p645]

waitingonprometric  Also, rule out cancers because no weight loss, symptoms are not constant throughout month, and symptoms are not getting progressively worse over the 2-yr history of pain +6  
cheesetouch  FA2018 P630 +2  


submitted by cassdawg(1165),

She has a craniopharyngioma, the most common childhood supratentorial tumor which is derived from remnants of Rathke's pouch (FA2020 p528). Craniopharyngiomas commonly have calcification and can cause hypopituitary issues (like low HGH). Suprasellar is also the location of the pituitary, and pituitary tumors in general cause bitemporal hemianopsia due to compression of the optic chiasm.

Rathke's pouch (where craniopharyngiomas and anterior pituitary are derived from) is derived from the surface ectoderm of the oral cavity.

Note that the neurohypophysis (posterior pituitary) is derived from neural ectoderm while the adenohypophysis (anterior pituitary) is derived from surface ectoderm of the oral cavity.

waitingonprometric  If you can recognize that this is a craniopharyngioma based on "calcified cystic mass in the suprasellar region," then you can think "cranio-" mass in the brain, "-pharyngioma" from structures connected to the mouth. Always works for me! +6  
cheesetouch  FA 2018 P512 +1  


submitted by cassdawg(1165),

This is a choriocarcinoma, or a rare malignant trophoblastic tumor developed during/after pregnancy [FA2020 p642]. It is characterized by increased serum beta hCG and "cannonball" metastases to the lung. Biopsy would show trophoblastic tissue with no chorionic villi present.

cheesetouch  Fa 2018 p 622 +2  


From FA2020, pg. 381:

Tubular adenoma--> neoplastic; tubular histology has less malignant potential than villous; tubulovillous has intermediate malignant potential; usually asymptomatic, may present with rectal bleeding. Hence our patient who has been undergoing evaluation for fecal occult blood.

Other answers:

Hyperplastic polyp--> most common, generally smaller and in rectosigmoid region. I'm guessing the picture attached to this question is trying to clue us into this not being a small lesion.

Inflammatory pseudopolyps--> due to mucosal erosion in inflammatory bowel disease. There is no appreciable erosions in this picture, also the mass appears pedunculated, so we know it's not a spot of normal mucosa that just looks raised compared to surrounding erosion.

Juvenile polyp and Peutz-Jeghers syndrome--> these are both genetic disorders with numerous hamartomatous polyps seen in the colon. Peutz-Jeghers also associated with increased risk of breast and other GI cancers. It is unlikely that our patient had either of these b/c he is 70 y/o; therefore, if he had one of these, he would likely have more than one colon lesion and may also present with a history of other cancers at his age.

cheesetouch  great refutation of others, thanks! +2  
lpp06  To add - tubular adenomas are pedunculate masses, as seen in the image +2  
soccerfan23  great explanation and username lol +  
sexymexican888  Also... idk if this helps but it got me the right answer (plus clinical scenario) : golijan said TUBULAR ADENOMA -> STRAWBERRY ON A STICK I know thats for the histology but idk thats what it looked like to me haha +  


submitted by lfcdave182(32),

Pg 366 FA 2020.

  • Below pectinate line: External hemorrhoids: Painful if thrombosed: Inferior Rectal Vein.
neovanilla  Note: pg 365 FA 2020 states: anorectal varices: portal <--> systemic: superior rectal <--> middle and inferior rectal. Not sure if that's correct, but definitely the info cited in pg 366 is correct +1  
cheesetouch  FA 2018 p360 +  


submitted by cassdawg(1165),

Atrial myxomas are the most common cardiac tumor in adults, and they may cause embolus complications hence our lady's painless loss of vision, likely due to central retinal artery occlusion [FA2020 p316]

The histology is characteristic of a myxoma with gelatinous material and cells immersed in glycosaminoglycans.

According to Daddy Goljan, basically for primary heart tumors if its an adult its a myxoma, if its a kid its a rhabdomyoma.

cheesetouch  FA20118 P309 +  
bingcentipede  It's also in the LEFT ATRIUM! +2  


submitted by cassdawg(1165),

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)

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


I think that this is osteogenesis imperfecta based on the hx of several fractures that occurred during birth.

From FA2019, pg. 51: Manifestations can include--multiple fractures with bone deformities and minimal trauma; may occur during the birth process

OI is caused by gene defects in COL1A1 and COL1A2; most common form is autosomal dominant with decreased production of normal type 1 collagen.

cheesetouch  OI does have macrocephaly https://rarediseases.org/rare-diseases/osteogenesis-imperfecta/ +2  
cheesetouch  FA2018 P 51 +  
peteandplop  If you've ever seen Unbreakable, the main villain (Mr. Glass) has OI and is born with many broken bones--memorable scene to remember this disease (https://youtu.be/5E69-oJ7TDc?t=100); Other memory device, OI = bONEs for Collagen Type ONE +7  
jurrutia  But what explains the poor skull mineralization? OI does not affect mineralization. +  


I think that this is osteogenesis imperfecta based on the hx of several fractures that occurred during birth.

From FA2019, pg. 51: Manifestations can include--multiple fractures with bone deformities and minimal trauma; may occur during the birth process

OI is caused by gene defects in COL1A1 and COL1A2; most common form is autosomal dominant with decreased production of normal type 1 collagen.

cheesetouch  OI does have macrocephaly https://rarediseases.org/rare-diseases/osteogenesis-imperfecta/ +2  
cheesetouch  FA2018 P 51 +  
peteandplop  If you've ever seen Unbreakable, the main villain (Mr. Glass) has OI and is born with many broken bones--memorable scene to remember this disease (https://youtu.be/5E69-oJ7TDc?t=100); Other memory device, OI = bONEs for Collagen Type ONE +7  
jurrutia  But what explains the poor skull mineralization? OI does not affect mineralization. +  


submitted by cheesetouch(140),

odds ratio for the exposure variable (aniline dye) = (yes cancer and yes dye / yes dye) / (no cancer and yes dye / yes dye) = (250/250) / (50/150) = 3

cheesetouch  FA 2018 P 254 +1  
cheesetouch  oops messed up the denominator a bit. 50/150 = (no cancer yes dye / no cancer no dye) +  


submitted by cheesetouch(140),

odds ratio for the exposure variable (aniline dye) = (yes cancer and yes dye / yes dye) / (no cancer and yes dye / yes dye) = (250/250) / (50/150) = 3

cheesetouch  FA 2018 P 254 +1  
cheesetouch  oops messed up the denominator a bit. 50/150 = (no cancer yes dye / no cancer no dye) +  


submitted by cassdawg(1165),

FA2020 p258

Odds ratio = (250/250) / (50/150) = 3

cheesetouch  FA 2018 P254 +1  
bingcentipede  For OR = ad/bc (from a/c divided by b/d) +  


submitted by cassdawg(1165),

Monoclonal antibodies used for inflammatory bowel disease include infliximab and adalimumab, both of which are directed against TNFalpha (FA2020 p382, 122, 487)

Another way of thinking about this is to think about common therapeutic antibodies used as well as the function of the other things listed to eliminate them. TNFalpha is commonly blocked by biologics for therapy in autoimmune and inflammatory disease, and generally it makes sense it would be beneficial to block as it is one of the primary pro-inflammatory cytokines

Bradykinin is involved in inflammation but has no major therapeutic Abs targeting it. C5a is an anaphylotoxin, and though monoclonal antibodies targeting C5 do exist they are used to treat paroxysmal noturnal hemoglobinuria. C5a does not play a major role in the pathogenesis of IBD. Blocking class I MHC antigens does not make sense, as antigens are what elicit the immune response and are presented to T-cells and there are millions of possible antigens that could be presented that are eliciting the inflammatory response. If you block class I MHC ittself it would also be extremely detrimental as then CD8 T-cells would not be able to respond to any infection/etc. Fibrin is involved in the clotting pathway and would not be beneficial to block in IBD. PGE2 is associated with pain, but it is not targeted by any therapeutic antibodies.

cheesetouch  FA P472 adalimumab/infliximab Anti-TNF-a monoclonal Ab +  


submitted by cassdawg(1165),

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.

cheesetouch  FA 2018 p218 +1  


submitted by cassdawg(1165),

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.

zalzale96  Created an account just to up vote this answer +4  
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. +3  
ownersucks  This question presentation is exactly how Sattar said in pathoma Ch2. Raise in cardiac enzyme following reperfusion +