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 +1  (nbme24#32)

suspensory ligament has ovarian vessels --> ovarian artery + ureter can be damaged in oophorectomy

cardinal ligament has uterine vessels --> uterine artery + ureter can be damaged in hysterectomy


 +0  (nbme24#32)

suspensory ligament has ovarian vessels --> ureter can be damaged in oophorectomy

cardinal ligament has uterine vessels --> ureter can be damaged in hysterectomy


 +0  (nbme24#1)

macrocytic anemia (seen in blood smear) = RBC precursors can grow but not divide

oval macrocytes (seen in blood smear) = megaloblastic anemia (if they don't show neutrophil hypersegmentation)

B12 has neurologic symptoms and low methylmalonic acid while folate deficiency does not

folate is absorbed in jejunum, B12 in ileum

causes of B12 deficiency = pernicious anemia, gastrectomy, ileal resection, fish tapeworm, veganism

D) failure of MTHFR --> THF (via methyltransferase = B12 deficiency and macrocytic anemia

B) G6PD deficiency = normocytic because of incr RBC destruction; pt would show intravascular hemolysis sx precipitated by an oxidative stressor

C) protoporphyinogen oxidase deficiency = microcytic anemia because of low heme synthesis

A) decr transferrin = high ferritin = anemia of chronic disease = microcytic anemia because of low iron


 +0  (nbme24#6)

acute exacerbation of CHF leads to reduced CO --> hypervolemic hyponatremia, body perceives it as hypovolemic (so you expect high ADH) ["non-osmotic release of ADH"]

  • this pt is clinically hypervolemic (edema, rales, distended neck veins)

  • urine should be concentrated (UOsm >100 mOsm/kg) because kidneys should be fine and ADH is doing its job, just with bad information

  • if urine is dilute, it's not CHF, it's psychogenic (can be caused by schizophrenia or factitious disorder)

let's say she wasn't crazy and really was having CHF exacerbation - tx with diuretic and fluid restriction as they did--> note that you can also use vaptan drugs for CHF-related hyponatremic hypervolemia (block ADH) --> should cause the urine to be dilute which will reduce the hypervolemia and reduce salt resorption to correct the hyponatremia

random diabetes inspidius side note for psychogenic polydipsia (DI dx is hypernatremia/normal, hypovolemia, dilute urine <100mOsm/kg)

  • can also use the water deprivation test for a pt with polyuria and polydipsia

--> if urine concentrates, it's psychogenic

--> if it does not concentrate, give desmopressin and if it concentrates = central DI, does not concentrae = nephrogenic DI


 +0  (nbme24#45)

ADA mutation = autosomal recessive SCID

IL-2-R gamma chain mutation = XLR SCID

IL-2-R alpha chain (CD25) = T-reg dysfunction; assoc with autoimmunity esp. T1DM, MS

Fas ligand (CD95) mutation = no T cell apoptosis in negative selection in thymic medulla = incr circulation of self-reacting lymphocyte = autoimmune lymphoproliferative syndrome


 +0  (nbme24#30)

epi = pheochromocytoma of adrenal medulla = episodic HTN PTHrP = squamous cell carcinoma of lung (plus others) = hypercalcemia VIPoma = neuroendocrine pancreatic tumor =secretory diarrhea [WDHA (watery diarrhea, hypokalemia, achlorhydia]


 +0  (nbme24#4)

A = CN III

B = CN V

C = CN VI

D = CN VII

E = CN VIII

F = CN X


 +1  (nbme24#36)

pharm causes of pill-induced esophagitis = bisphosphonates, tetracyclines, NSAIDs, iron, potassium chloride

bisphosphonates MOA = bind hydroxapatite to reduce osteoclast activity (used in osteoporosis, Paget disease of bone, osteogenesis imperfecta, hypercalcemia and mets to bone)

osteoporosis pharm

  1. Ca2+/Vit D supplementation (prophylaxis)

  2. bisphosphonates - ADMEs = esophagitis, ONJ, atypical femoral stress fractures

  3. pulsatile PTH analogs (teriparatide) = only one that incr bone growth (stimulates osteoblasts) --> transient hypercalcemia, also incr risk of osteosarcoma (dont give to paget dz of bone or any cancer pt)

  4. SERM (raloxifene = antagonist at breasts and uterus, AGONIST at bone = no incr risk of endometrial hyperplasia...but still incr risk of thromboembolism)

  5. denosumab (mab against RANKL i.e. mimics OPG)

  6. rarely calcitonin

sunshinesweetheart  IGNORE ALLLLL MY OTHER POSTS lol I just learned text boxes. brb will continue helping no one/jumping out a window

 +0  (nbme24#36)

pharm causes of pill-induced esophagitis = bisphosphonates, tetracyclines, NSAIDs, iron, potassium chloride

bisphosphonates MOA = bind hydroxapatite to reduce osteoclast activity (used in osteoporosis, Paget disease of bone, osteogenesis imperfecta, hypercalcemia and mets to bone)

osteoporosis pharm

  1. Ca2+/Vit D supplementation (prophylaxis)

  2. bisphosphonates - pulsatile PTH analogs (teriparatide) = only one that incr bone growth (stimulates osteoblasts) --> transient hypercalcemia, also incr risk of osteosarcoma (dont give to paget dz of bone or any cancer pt)

  3. SERM (raloxifene = antagonist at breasts and uterus, AGONIST at bone = no incr risk of endometrial hyperplasia...but still incr risk of thromboembolism)
  4. denosumab (mab against RANKL i.e. mimics OPG) - rarely calcitonin
sunshinesweetheart  GOT IT IN LIST FORM #procrastinating

 +0  (nbme24#36)

pharm causes of pill-induced esophagitis = bisphosphonates, tetracyclines, NSAIDs, iron, potassium chloride

bisphosphonates MOA = bind hydroxapatite to reduce osteoclast activity (used in osteoporosis, Paget disease of bone, osteogenesis imperfecta, hypercalcemia and mets to bone)

osteoporosis pharm 1. Ca2+/Vit D supplementation (prophylaxis) 2. bisphosphonates - pulsatile PTH analogs (teriparatide) = only one that incr bone growth (stimulates osteoblasts) --> transient hypercalcemia, also incr risk of osteosarcoma (dont give to paget dz of bone or any cancer pt) 3. SERM (raloxifene = antagonist at breasts and uterus, AGONIST at bone = no incr risk of endometrial hyperplasia...but still incr risk of thromboembolism) 4. denosumab (mab against RANKL i.e. mimics OPG) - rarely calcitonin

sunshinesweetheart  ha I am bad at using websites and can't make this a list that doesn't transform into a paragraph :( sorry

 +0  (nbme24#36)

pharm causes of pill-induced esophagitis = bisphosphonates, tetracyclines, NSAIDs, iron, potassium chloride

bisphosphonates MOA = bind hydroxapatite to reduce osteoclast activity (used in osteoporosis, Paget disease of bone, osteogenesis imperfecta, hypercalcemia and mets to bone)

osteoporosis pharm - Ca2+/Vit D supplementation (prophylaxis) - bisphosphonates - pulsatile PTH analogs (teriparatide) = only one that incr bone growth (stimulates osteoblasts) --> transient hypercalcemia, also incr risk of osteosarcoma (dont give to paget dz of bone or any cancer pt) - SERM (raloxifene = antagonist at breasts and uterus, AGONIST at bone = no incr risk of endometrial hyperplasia...but still incr risk of thromboembolism) - denosumab (mab against RANKL i.e. mimics OPG) - rarely calcitonin


 +0  (nbme24#38)

p 619 FA 2019 - physiologic changes in pregnancy

incr CO, anemia, hypercoagulability, hyperventilation, incr lipoylsis and fat utilization to preserve glucose and AAs for the baby


 +0  (nbme24#46)

some fun facts 4 u hoes to rule out the wrong answers:

Arcuate nucleus aka “infundibular nucleus” = hypothalamic nucleus. Projects dopaminergic neurons to anterior pituitary gland --> inhibits PRL. One of the 4 main dopamine pathways of the brain. Prolactin also gives feedback and inr dopamine secretion via this pathway [p 487 FA 2019]

Frontal cortex = oligodendrioma [p 514 FA 2019] rare, slow growing, fried egg appearance, may present with seizures

pituitary adenoma [p 514 FA 2019] - Bitemporal hemianopia - Most commonly a prolactinoma (hyperplasia of lactotrophs) - Male: decr libido, infertility - Female: galactorrhea, amenorrhea (PRL negative feedback on hypothalamic GnRH) - Can also see hyperplasia of somatotrophs (GH) --> acromegaly, gigantism or corticotrophs --> Cushing disease

PPRF = in charge of eye movements/conjugate gaze [p 503 FA 2019] - A stroke by the basilar artery of circular willis will lead to loss of horizontal, but not vertical eye movements


 +0  (nbme24#7)

"purplish" is a frustrating word here but they key is CAVERNOUS VASCULAR CHANNELS. Port wine stain in sturge weber and salmon patch ("stork bite") are both flat lesions, not a hemangioma.

sunshinesweetheart  outcomes: stork bite/salmon patch will regress by 5-6year old or persist into adulthood; strawberry hemangioma will regress by 3-6 year old; port wine stain will regress or persist but it'll be associated with the sturge-weber stuff see the mnemonic pg 513 of FA 2019)
sunshinesweetheart  oops correction on port wine stain outcome: "lesions become a deeper purple, and angiomatous bleeding papules and soft tissue hypertrophy often develop. Because of the propensity of these cutaneous lesions to persist and grow, treatment of cosmetically or functionally impairing port-wine stains is recommended during infancy to prevent the soft tissue and bony changes" from the link kateinwonderland posted above

 +0  (nbme24#10)

look at FA 2019 pg. 261

in a Gaussian, 66% are within 1 SD and 95% within 2 SD

this is high yield af


 +0  (nbme24#3)

out of curiosity, why are AST and ALT high? is that saying the NRTI used was diadenosine which led to pancreatitis also?

krewfoo99  AST and ALT will not be elevated in pancreatitis, they will only be increased during liver damage. NRTI causes hepatoxicity (although FA 2018 states NNRTI causes hepatotoxicity, NRTI could also be an option considering the two classes are similar. The hepatoxicity will cause an increase in ALT and AST




Subcomments ...

submitted by neonem(262),

Pg 491 in FA 2018 (Neurology anatomy & physiology section): 3 muscles close the jaw: Masseter, teMporalis, Medial pterygoid 1 muscle opens the jaw: Lateral pterygoid ALL are innervated by trigeminal nerve, V3 Mnemonic: M's munch (close the jaw), L's lower (loosen/relax the jaw)

sunshinesweetheart  p 495 in FA 2019 +  


submitted by brethren_md(44),

Classic sleep apnea in the patient. Cessation of breathing causes nocturnal hypoxia and systemic hypertension/arrhythmic/sudden death can persist. PaO2 is normal during day and decreased during episodes and at night. Classically seen in Obese patients such as the patient in the question stem.

tinydoc  Caused a cessation of breathing rather than a ↓ in lung volume although a patient could develop an obesity related restrictive lung disease thats not whats happening with this question. +  
sunshinesweetheart  p 665 FA 2019 +  


submitted by sajaqua1(212),

Primary prevention is an active step taken to head off or mitigate a disease- think of vaccinations. In this case, it is lifestyle modification (exercise) to help 30-40 year old women (weight bearing exercise can mitigate osteoporosis, benefits of aerobic exercise).

Seconday prevention is early detection of a disease, promoting early intervention. This could inclue things like HIV testing every 6 months, or or annual mammography.

Tertiary intervention is therapy aiming at reducing complications, allowing relapse, or improving function. Abstinence from alcohol may be here because of substance abuse problems, or because some damage previously done by alcohol cannot be prevented. Similarly for a low carbohydrate diet we may be mitigating the effects on metabolism that have already been done.

sunshinesweetheart  p 269 FA 2019 +  


submitted by famylife(37),

To rule out SIADH type: "Serum potassium concentration generally remains unchanged. Movement of potassium from the intracellular space to the extracellular space prevents dilutional hypokalemia. As hydrogen ions move intracellularly, they are exchanged for potassium in order to maintain electroneutrality."

https://www.medscape.com/answers/246650-8383/how-does-syndrome-of-inappropriate-antidiuretic-hormone-secretion-siadh-affect-serum-potassium-levels

usmile1  Does anyone know if SIADH is associated with hypertension? I don't think it is due to the body's response of downregulating aldosterone, but if someone could verify that I would appreciate it. +  
sunshinesweetheart  @usmile1 pg 579 FA 2019 = BP can be normal or high in SIADH +  


submitted by m-ice(124),

Question is basically asking what are the substrates used the first step in heme synthesis. In that step, glycine and succinyl CoA are combined to make aminolevulinic acid.

sunshinesweetheart  p 417 FA 2019 +  


pharm causes of pill-induced esophagitis = bisphosphonates, tetracyclines, NSAIDs, iron, potassium chloride

bisphosphonates MOA = bind hydroxapatite to reduce osteoclast activity (used in osteoporosis, Paget disease of bone, osteogenesis imperfecta, hypercalcemia and mets to bone)

osteoporosis pharm

  1. Ca2+/Vit D supplementation (prophylaxis)

  2. bisphosphonates - ADMEs = esophagitis, ONJ, atypical femoral stress fractures

  3. pulsatile PTH analogs (teriparatide) = only one that incr bone growth (stimulates osteoblasts) --> transient hypercalcemia, also incr risk of osteosarcoma (dont give to paget dz of bone or any cancer pt)

  4. SERM (raloxifene = antagonist at breasts and uterus, AGONIST at bone = no incr risk of endometrial hyperplasia...but still incr risk of thromboembolism)

  5. denosumab (mab against RANKL i.e. mimics OPG)

  6. rarely calcitonin

sunshinesweetheart  IGNORE ALLLLL MY OTHER POSTS lol I just learned text boxes. brb will continue helping no one/jumping out a window +1  


pharm causes of pill-induced esophagitis = bisphosphonates, tetracyclines, NSAIDs, iron, potassium chloride

bisphosphonates MOA = bind hydroxapatite to reduce osteoclast activity (used in osteoporosis, Paget disease of bone, osteogenesis imperfecta, hypercalcemia and mets to bone)

osteoporosis pharm

  1. Ca2+/Vit D supplementation (prophylaxis)

  2. bisphosphonates - pulsatile PTH analogs (teriparatide) = only one that incr bone growth (stimulates osteoblasts) --> transient hypercalcemia, also incr risk of osteosarcoma (dont give to paget dz of bone or any cancer pt)

  3. SERM (raloxifene = antagonist at breasts and uterus, AGONIST at bone = no incr risk of endometrial hyperplasia...but still incr risk of thromboembolism)
  4. denosumab (mab against RANKL i.e. mimics OPG) - rarely calcitonin
sunshinesweetheart  GOT IT IN LIST FORM #procrastinating +  


pharm causes of pill-induced esophagitis = bisphosphonates, tetracyclines, NSAIDs, iron, potassium chloride

bisphosphonates MOA = bind hydroxapatite to reduce osteoclast activity (used in osteoporosis, Paget disease of bone, osteogenesis imperfecta, hypercalcemia and mets to bone)

osteoporosis pharm 1. Ca2+/Vit D supplementation (prophylaxis) 2. bisphosphonates - pulsatile PTH analogs (teriparatide) = only one that incr bone growth (stimulates osteoblasts) --> transient hypercalcemia, also incr risk of osteosarcoma (dont give to paget dz of bone or any cancer pt) 3. SERM (raloxifene = antagonist at breasts and uterus, AGONIST at bone = no incr risk of endometrial hyperplasia...but still incr risk of thromboembolism) 4. denosumab (mab against RANKL i.e. mimics OPG) - rarely calcitonin

sunshinesweetheart  ha I am bad at using websites and can't make this a list that doesn't transform into a paragraph :( sorry +  


submitted by drmomo(2),

why can't it be culex mosquito? maybe wuchereria bancrofti filariasis?

sunshinesweetheart  diff presentation - that's elephentiasis +  
sunshinesweetheart  plus filariasis isn't the same as microfilariae +  


submitted by drmomo(2),

why can't it be culex mosquito? maybe wuchereria bancrofti filariasis?

sunshinesweetheart  diff presentation - that's elephentiasis +  
sunshinesweetheart  plus filariasis isn't the same as microfilariae +  


Why is it not ovarian follicle cells? I thought the female analog of Sertoli and Leydig is theca/granulosa cells.

colonelred_  Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen. +2  
brethren_md  Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen +1  
sympathetikey  Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen +1  
s1q3t3  Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen +1  
masonkingcobra  Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen +  
mcl  Wait, but did anyone mention that females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen??? +10  
mcl  But seriously though, pathology outlines says sertoli-leydig tumor "may be suspected clinically in a young patient presenting with a combination of virilization, elevated testosterone levels and ovarian / pelvic mass on imaging studies." As for follicle cell tumors, granulosa cell tumors usually occur in adults and would cause elevated levels of estrogens. Theca cell tumor would also primarily produce estrogens. Putting the links at the end since idk if they're gonna turn out right lol Link pathology outlines for sertoli leydig granulosa cell tumor theca cell tumor +6  
bigjimbo  LOL +  
fallenistand  Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen. +2  
medpsychosis  So after doing some intense research, UPtoDate, PubMed, an intense literature review on the topic I have come to the final conclusion that...... ...... ...... ...... Wait for it.... ..... ..... Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen. +3  
charcot_bouchard  Hello, i just want to add that Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen +1  
giggidy  Hold up, so I'm confused - I read all the posts above but I still am unsure - are sertoli-leydig cells notorious for producing androgen? +1  
subclaviansteele  Hold the phone.....Females can get sertoli leydig cell tumors which are notorious for producing androgen? TIL TL;DR - Females can get sertoli leydig cell tumors = high androgens +  
cinnapie  I just found a recent study on PubMed saying "Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen" +  
youssefa  Hahahahaha ya'll just bored +2  
water  Bored? you wouldn't think so if you knew that females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen +  
nbmehelp  I dont get it +  
redvelvet  how don't you get it that females can get Sertoli Leydig cell tumors, which are notorious for producing lots of androgen? +  
drmomo  what if this means..... females can get Sertoli Leydig cell tumors, which are notorious for producing lots of androgen +  
sunshinesweetheart  hahahaha this made my day #futurephysicians #lowkeyidiots +  
sunshinesweetheart  @medstruggle look up placental aromatase deficiency (p. 625 FA 2019), it would have a different presentation +  
deathbystep1  i am sure i would ace STEP 1 if i only knew that females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen +  
noplanb  Wait... I might actually never forget this now lol +  


Why is it not ovarian follicle cells? I thought the female analog of Sertoli and Leydig is theca/granulosa cells.

colonelred_  Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen. +2  
brethren_md  Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen +1  
sympathetikey  Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen +1  
s1q3t3  Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen +1  
masonkingcobra  Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen +  
mcl  Wait, but did anyone mention that females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen??? +10  
mcl  But seriously though, pathology outlines says sertoli-leydig tumor "may be suspected clinically in a young patient presenting with a combination of virilization, elevated testosterone levels and ovarian / pelvic mass on imaging studies." As for follicle cell tumors, granulosa cell tumors usually occur in adults and would cause elevated levels of estrogens. Theca cell tumor would also primarily produce estrogens. Putting the links at the end since idk if they're gonna turn out right lol Link pathology outlines for sertoli leydig granulosa cell tumor theca cell tumor +6  
bigjimbo  LOL +  
fallenistand  Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen. +2  
medpsychosis  So after doing some intense research, UPtoDate, PubMed, an intense literature review on the topic I have come to the final conclusion that...... ...... ...... ...... Wait for it.... ..... ..... Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen. +3  
charcot_bouchard  Hello, i just want to add that Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen +1  
giggidy  Hold up, so I'm confused - I read all the posts above but I still am unsure - are sertoli-leydig cells notorious for producing androgen? +1  
subclaviansteele  Hold the phone.....Females can get sertoli leydig cell tumors which are notorious for producing androgen? TIL TL;DR - Females can get sertoli leydig cell tumors = high androgens +  
cinnapie  I just found a recent study on PubMed saying "Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen" +  
youssefa  Hahahahaha ya'll just bored +2  
water  Bored? you wouldn't think so if you knew that females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen +  
nbmehelp  I dont get it +  
redvelvet  how don't you get it that females can get Sertoli Leydig cell tumors, which are notorious for producing lots of androgen? +  
drmomo  what if this means..... females can get Sertoli Leydig cell tumors, which are notorious for producing lots of androgen +  
sunshinesweetheart  hahahaha this made my day #futurephysicians #lowkeyidiots +  
sunshinesweetheart  @medstruggle look up placental aromatase deficiency (p. 625 FA 2019), it would have a different presentation +  
deathbystep1  i am sure i would ace STEP 1 if i only knew that females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen +  
noplanb  Wait... I might actually never forget this now lol +  


submitted by neonem(262),

this patient has symptomatic aortic stenosis. This can be identified by the ventricular hypertrophy (to compensate for increased functional afterload from non-compliant aortic valve), midsystolic murmur and the location at the normal aortic area.

Per UpToDate on Clinical manifestations of Aortic Stenosis:

"Dizziness and syncope — Syncope occurs as a presenting symptom in approximately 10 percent of patients with symptomatic severe AS (or approximately 3 percent of all patients with severe AS) [3]. There are several proposed explanations for exertional dizziness (presyncope) or syncope in patients with AS, both of which reflect decreased cerebral perfusion. Exercise-induced vasodilation in the presence of an obstruction with fixed cardiac output can result in hypotension."

guillo12  What does "fixed cardiac output" signify? +  
usmleuser007  "fixed cardiac output" might mean that with the stenosis (ie. narrowed aortic valve) there is a limited or rather reduced cardiac output. Exercise would not increase cardiac output because the stenosis is caused by a mechanical (physical) rather than a biochemical process. Therefore, At any given moment the heart can not increase its output no matter how forcefully it contracts. +1  
fallot4logy  why not option A?arterial compression ? +  
sunshinesweetheart  @fallot4logy LVH does not lead to coronary artery compression. only reallyyyy rarely will pulmonary artery dilation cause coronary artery compression. plus that would cause angina but probably wouldnt decrease cerebral bloodflow to syncope. her murmur + LVH point us toward aortic stenosis which does cause those --> fixed CO +  


submitted by yotsubato(282),

Amyloid A : seen in chronic inflammatory conditions, deposition of amyloid in tissues

B2 microglobulin: associated with ESRD and long term dialysis

Neurofilament protein: Form the cytoskeleton of neurons (in healthy individuals)

Presenilin: associated with familial alzheimers disease

sunshinesweetheart  neurofilament also seen in neuronal tumors i.e. neuroblastoma +  


submitted by xxabi(95),

Stent thrombosis vs re-stenosis. Stent thrombosis is an acute occlusion of a coronary artery stent, which often results in acute coronary syndrome. Can be prevented by dual antiplatelet therapy or drug-eluting stents. Re-stenosis is the gradual narrowing of the stent lumen due to neointimal proliferation, resulting in anginal symptoms.

sunshinesweetheart  so just to clarify - it's the "symptom-free for 3 months" that rules out thrombosis? +1  
hpsbwz  It's moreso that at rest there's no changes, but during exercise there is. Like the pathophys of stable angina. +  


"purplish" is a frustrating word here but they key is CAVERNOUS VASCULAR CHANNELS. Port wine stain in sturge weber and salmon patch ("stork bite") are both flat lesions, not a hemangioma.

sunshinesweetheart  outcomes: stork bite/salmon patch will regress by 5-6year old or persist into adulthood; strawberry hemangioma will regress by 3-6 year old; port wine stain will regress or persist but it'll be associated with the sturge-weber stuff see the mnemonic pg 513 of FA 2019) +  
sunshinesweetheart  oops correction on port wine stain outcome: "lesions become a deeper purple, and angiomatous bleeding papules and soft tissue hypertrophy often develop. Because of the propensity of these cutaneous lesions to persist and grow, treatment of cosmetically or functionally impairing port-wine stains is recommended during infancy to prevent the soft tissue and bony changes" from the link kateinwonderland posted above +  


"purplish" is a frustrating word here but they key is CAVERNOUS VASCULAR CHANNELS. Port wine stain in sturge weber and salmon patch ("stork bite") are both flat lesions, not a hemangioma.

sunshinesweetheart  outcomes: stork bite/salmon patch will regress by 5-6year old or persist into adulthood; strawberry hemangioma will regress by 3-6 year old; port wine stain will regress or persist but it'll be associated with the sturge-weber stuff see the mnemonic pg 513 of FA 2019) +  
sunshinesweetheart  oops correction on port wine stain outcome: "lesions become a deeper purple, and angiomatous bleeding papules and soft tissue hypertrophy often develop. Because of the propensity of these cutaneous lesions to persist and grow, treatment of cosmetically or functionally impairing port-wine stains is recommended during infancy to prevent the soft tissue and bony changes" from the link kateinwonderland posted above +  


submitted by neonem(262),

Lack of CD18 (LFA-1 integrin) on phagocytes is the cause of leukocyte adhesion deficiency type 1 (LAD1). Since phagocytes like neutrophils and macrophages can't get out of the bloodstream, they are stuck in the blood, hence the leukocytosis with WBC count > 10,000. Since the leukocytes are stuck in the blood, they can't mount an effective immune response against bacteria.

sunshinesweetheart  also for completeness, LFA-1 is an integrin that binds ICAM, so LAD1 results from a defect in tight binding +  


submitted by happysingh(7),

so, the Key words that no one is mentioning : communicating hydrocephalus

the pathophys goes like this :

an inflammatory setting (i.e., subarachnoid hemorrhage) yield fibrosis / scarring of the arachnoid granulations => impaired CSF drainage

the key points / concepts they are trying to test here : 1. do you know what communicating hydrocephalus (without them telling you those words) 2. do you know what's the pathophysiology (of communicating hydrocephalus) is ?

potentialdoctor1  Exactly. To add to this, communicating hydrocephalus can be subdivided as follows: Normal-pressure hydrocephalus: Chronic/gradual decrease in CSF reabsorption at arachnoid granulations, usually due to calcification due to aging. CSF accumulates slowly, so ventricles are able to widen without causing an important increase in intracranial pressure. Symptoms occur due to compression of periventricular white matter tracts ---> Wacky, wobbly, wet High-pressure hydrocephalus: Acute decrease in CSF reabsorption at arachnoid granulations, usually due to inflammatory state in the subarachnoid space (eg, meningitis, sub-arachnoid hemorrhage). CSF accumulates suddenly, causing an acute-onset increase in intracranial pressure +2  
sunshinesweetheart  not to take away from your perfect explanations, but if it were a woman with neck stiffness and fever (rather than circle of willis rupture) that could lead to increased CSF production, right? I think that's the only case where CSF production would increase. Also I think decr absorption in arachnoid granulations in that situation as well so it'd be a shit question +  


Why not clinical trial? They could report a rare adverse effect in phase 4 clinical trial right?

sunshinesweetheart  there's no control group. it's just a case study. x3 +  
sunshinesweetheart  plus clinical trials at that stage would have had tons and tons of participants (and, most importantly to rule out all the answers, control group) +  


Why not clinical trial? They could report a rare adverse effect in phase 4 clinical trial right?

sunshinesweetheart  there's no control group. it's just a case study. x3 +  
sunshinesweetheart  plus clinical trials at that stage would have had tons and tons of participants (and, most importantly to rule out all the answers, control group) +  


submitted by m-ice(124),

The patient needs medical attention immediately, which eliminates obtaining a court order, or transferring her. A nurse does not have the same training and qualifications as a physician, so it would be inappropriate to ask them to examine the patient. Asking the hospital chaplain again could be inappropriate, and would take more time. Therefore, the best option among those given is to ask the patient if she will allow with her husband present.

sympathetikey  Garbage question. +17  
masonkingcobra  So two men is better than one apparently +5  
zoggybiscuits  GarBAGE! ? +  
bigjimbo  gárbágé +  
fulminant_life  this question is garbage. She doesnt want to be examined by a male how would the presence of her husband make any difference in that respect? +1  
dr.xx  I guess this is a garbage question because what hospital, even small and rural, does not have a female physician on staff. NBME take notice -- this is the 2010s not 1970s. https://images.app.goo.gl/xBL4cK31ta7nG4L39 +1  
medpsychosis  The question here focuses on a specific issue which is the patient's religious conservative beliefs vs. urgency of the situation. A physician is required to respect the patient's autonomy while also balancing between beneficence and non-maleficence. The answer choice where the physician asks the patient if it would be ok to perform the exam with the husband present is an attempt to respect the conservative religious belief of the patient (not being exposed or alone with another man in the absence of her husband) while also allowing the physician to provide necessary medical treatment that could be life saving for her and or the child. Again, this allows for the patient to practice autonomy as she has the right to say no. +5  
sahusema  I showed this question to my parents and they said "this is the kind of stuff you study all day?" smh +5  
sherry  I totally agree this is a garbage question. I personally think there is more garbage question on new NBME forms than the previous ones...they can argue in any way. I feel like they were just trying to make people struggle on bad options when everybody knows what they were trying to ask. +  
niboonsh  This question is a3othobillah +  
sunshinesweetheart  this question is really not that garbage....actually easy points I was grateful for... yall are just clearly ignorant about Islam. educate yourselves, brethren, just as this exam is trying to get you to do. but yeah I agree there should be an option for female physician lol +  


Can anybody explain this one? I put repeated tests because I assumed an 83-year-old woman is an unusual demographic for syphilis.

m-ice  83 might seem an uncommon age, but we don't know for sure her sexual history. She only recently (8 months ago) started showing some signs of mild cognitive impairment. She has all these results implying that she has syphilis, so the most likely answer is that she has syphilis, so we should speak to her privately about her sexual history. The tests don't necessarily means she got syphilis very recently, it's possible she's had syphilis for a while and never got treated. +2  
mousie  I understand that she could possibly have syphilis but I also put repeat tests because I know there are a few things that can cause false positive VRDLs but if she also has a + RPR does this make a FP less likely? And also if she has mild cognitive impairment you still discuss with her not her daughter correct ...? +2  
m-ice  This definitely could be a false positive, but before we want to consider it to be a false positive, we should talk to the patient about it privately. Assuming that it's a false positive before asking the patient about it could delay treatment of her syphilis. There's a chance she didn't want to disclose her sexual history in front of her daughter or maybe she was embarrassed or didn't think it was important to mention. And you're absolutely right, she only has mild cognitive impairment, so we most definitely should talk to the patient alone without her daughter first. +  
seagull  She has dementia. She doesn't have the capacity to determine her own care (23/20 MME). I feel the daughter should have the word on the care since Grandma likely doesn't have the capacity to understand her actions. +1  
sajaqua1  From what I remember, dementia is typically a combination of impaired memory *and* impaired thought processes. There is nothing to indicate that the patient has impaired thought processes, and the memory impairment is only mild. The patient can still reasonably said to be competent, and so her private information should be discussed with her alone. +6  
yotsubato  Elder care homes or elderly communities actually have a high rate of STDs. Turns out, when you put a bunch of divorced/widowed adults together in a community they have sex. +3  
yotsubato  Additionally, you should respect the privacy of a competent adult with "Mild memory" impairment. I know I could have mild memory impairment considering the crap I forget studying for step 1 +5  
drdoom  @seagull dementia ≠ absence of competence -- the two are separate concepts and have to be evaluated independently. see https://meshb.nlm.nih.gov/record/ui?ui=D003704 and https://meshb.nlm.nih.gov/record/ui?ui=D016743 +1  
wowo  also important to note, d) repeated tests is also incorrect as the microhemagglutination assay is a confirmatory treponemal test (along the same lines as FTA-ABS) https://www.uofmhealth.org/health-library/hw5839 +1  
sunshinesweetheart  also.... I think we can assume that "repeated tests" means repeat VRDL, not "additional tests to rule out false positives" +  


submitted by m-ice(124),

This woman has Paroxysmal Nocturnal Hemoglobinuria. This most often presents in a young adult who has episodes of dark urine in the middle of the night or when waking up in the morning. It's caused by complement activity directly against the patient's own RBCs. Certain glycolipids are needed on the RBC surface to prevent attack from complement, the most notable of which are CD55 and CD59. Patients with PNH have a somatic mutation in which they lost function of a PIGA enzyme needed for proper presentation and attachment of CD55/CD59 on the RBC surface. Therefore the answer is a defect in a cell membrane anchor protein. Without this, complement attacks RBCs.

usmleuser007  I knew the disorder and its pathophysiology. But sometimes the answer choices are so wordy or colorful that you still get it wrong.... +9  
sunshinesweetheart  I got this one right but now upon review I'm having trouble ruling out hereditary spherocytosis ("abnormal cell morphology") answer choice. It helps that the dark urine is in the mornings, but is it officially ruled out because of her age? like this is obvi an acquired mutation if someone's 33? +  
krewfoo99  @sunshinesweetheart Hereditary Spherocytosis is a autosomnal dominant condition. The patient in the question stem has had dark urine since the past 2 months (acute presentation). Since spherocytosis is hereditary, it wont be present as a acute condition +  


submitted by jkan(12),

c-peptide is low with exogenous insulin. (c-peptide made as a byproduct of insulin production in the body) repeated visits+ high insulin+low c-peptide= exogenous insulin abuse. In a child-> factitious by proxy

sunshinesweetheart  ugh, I feel like a child could misuse their insulin by accident without proper supervision. Totally thought she had T1DM and not enough guidance on how to use the meds. annoying +  


submitted by m-ice(124),

All HOX genes are transcription factors that help regulate body layout and different expression of genes for each body segment.

sunshinesweetheart  I got this one right but wasn't exactly sure how to rule out 'translation'. I guess just because we're talking about a gene i.e. trasncription and not miRNA i.e. post-translational modifiers? +