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 +0  (nbme24#31)

My understanding is that the pulmonary circulation changes very little in terms of an acute MI.

It is b/c pulmonary circulation has a lot more room to fill with blood much like the spleen in terms of blood accumulation.

With higher volume of blood in pulmonary circulation, more blood vessels are able to be recruited specially the apex.

With more recruited blood vessels = reduced pressure d/t circulation in parallel


 +3  (nbme24#37)

Simply put: more energy in a light wave the more likely it is to cause cellular (DNA) damage.

Ultraviolet has less energy than X-rays (it goes through your flesh to see bones!)

Order of light strength (cell damaging capability)

  • X-Ray > UVA (also able to cause double strand break) > UVB (most likely single strand break - repaired)

 +0  (nbme24#45)

Most absorption ad secretion is done at the PCT. It is this reason why the PCT is the most metabolically active portion of the nephron.

As this image shows, you can see that reabsorption & secretion occurs at the PCT

this means that both PAH & creatinine are secreted for elimination at the PCT along with the additional volume freely filtered through the bowman's capsule.

Furthermore; Inulin is neither secreted nor reabsorbed.

hence Inulin is better for GFR. But, creatinine is normally used for GFR as an estimate (probably d/t ease)


 +0  (nbme24#35)

After some research this is why the other answers are incorrect:

Basal keratinocyte & lamina lucida

  • Incorrect b/c lamina lucida is a component of the basement membrane which is found between the epithelium and underlying connective tissue (e.g., epidermis and dermis of the skin).
  • It is a roughly 40 nanometre wide electron-lucent zone between the plasma membrane of the basal cells and the (electron-dense) lamina densa of the basement membrane. (WIKI)
  • basal keratinocyte attaches to the basement membrane using hemidesmosome

Granular keratinocyte & stratum corneum

  • Stratum lucidum separates these two layers.
  • there are no desmosome that connect these two layers
  • Image for reference

Lamina lucida & Lamina densa -- click for image

  • both are part of the basement membrane and not the epidermis

Melanocyte & basal kertinocyte --- click for image

  • are both connected to eachoter via E-cadherins
  • it is probably the damage to this connection that

 +1  (nbme24#35)

After some research this is why the other answers are incorrect:

  1. basal keratinocyte & lamina lucida
  2. Incorrect b/c lamina lucida is a component of the basement membrane which is found between the epithelium and underlying connective tissue (e.g., epidermis and dermis of the skin).
  3. It is a roughly 40 nanometre wide electron-lucent zone between the plasma membrane of the basal cells and the (electron-dense) lamina densa of the basement membrane. (WIKI)
  4. basal keratinocyte attaches to the basement membrane using hemidesmosome

  5. Granular keratinocyte & stratum corneum

  6. Stratum lucidum separates these two layers.
  7. there are no desmosome that connect these two layers
  8. Image for reference

  9. Lamina lucida & Lamina densa -- click for image

  10. both are part of the basement membrane and not the epidermis

  11. Melanocyte & basal kertinocyte --- click for image

  12. are both connected to eachoter via E-cadherins
  13. it is probably the damage to this connection that might lead to melanoma

 +0  (nbme24#35)

Blistering diseases such as pemphigus vulgaris (PV) and pemphigus foliaceus (PF) are autoimmune diseases in which auto-antibodies target desmogleins.

  • PV is caused by circulating autoantibodies (IgG) that target Dsg3 (Desmoglein 3) and sometimes Dsg1.
  • PV is manifested by suprabasal acantholysis, or blisters in the mucous membrane and blisters in the epidermis.
  • PF patients have autoantibodies that target Dsg1 with superficial blisters on the epidermis with no mucous membrane issues.
  • Both disease result in a loss of keratinocyte adhesion.
  • Pemphigus can also be caused by a bacterial infection: bullous impetigo is an infection caused by a staphylococcus bacterium that releases a toxin that cleaves the Dsg1 extracellular domain.

 +2  (nbme24#34)

Some other endocrine like cells and disorders for reference:

  1. Salt-and-pepper chromatin (fine granular cytoplasm) in Endocrine tumors:

  2. Medullary thyroid carcinoma

  3. neuroendocrine tumors and pheochromocytoma
  4. Carcinoid Tumor (serotonin) --- (also has sheets of uniform cells)
  5. Small Cell Carcinoma of lungs = Small, blue cells with scant cytoplasm and granular chromatin) = flat, oval-shaped cells with scant cytoplasm and hyperchromatic nuclei

  6. Small Blue Cells

  7. Ewing sarcoma (anaplastic malignant tumor)
  8. SCC of lungs
  9. flat, oval-shaped cells with scant cytoplasm and hyperchromatic nuclei
happysingh  i've never heard of " 6. Small Blue Cells" cancer / tumor / carcinoma ....
niboonsh  might want to look at fa pg 665

 +5  (nbme23#23)
  1. Cancers of the pelvis, including the prostate, spread to the lumbosacral spine via the vertebral venous plexus (VVP).

    • The VVP communicates with a number of venous networks, including the prostatic venous plexus, which receives the venous supply from the prostate, penis, and bladder.

    • VVP runs up the entire spinal column and connects with the venous supply of the brain via a valveless system (Batson’s Plexus) which allows for bidirectional flow and regulation of intracranial pressure.This venous connection to the cerebral circulation may help explain the propensity of tumors to metastasize to the brain.

  2. The VVP also communicates with the azygos vein in the chest, which explains in part why breast and lung cancers frequently metastasize to the thoracic spine.

    • Similarly, due to pulmonary venous drainage into the left side of the heart, lung tumors often spread systemically via the arterial system.
  3. Although lymph nodes are the most common sites of metastasis in general, lymphatic spread to the skeletal system is very rare.

  4. The pampiniform plexus receives venous drainage from the testis, epididymis, and ductus deferens and drains into the testicular veins.


 +0  (nbme23#23) 3. Cancers of the pelvis, including the prostate, spread to the lumbosacral spine via the vertebral venous plexus(VVP).  a. The VVP communicates with a number of venous networks, i. including the prostatic venous plexus, which receives the venous supply from the prostate, penis, and bladder.  b. VVP runs up the entire spinal column and connects with the venous supply of the brain via a valveless system (Batson's Plexus) i. which allows for bidirectional flow and regulation of intracranial pressure.  ii. This venous connection to the cerebral circulation may help explain the propensity of tumors to metastasize to the brain. 4. The VVP also communicates with the azygos vein in the chest, which explains in part why breast and lung cancers frequently metastasize to the thoracic spine.  a. Similarly, due to pulmonary venous drainage into the left side of the heart, lung tumors often spread systemically via the arterial system. 5. Although lymph nodes are the most common sites of metastasis in general, lymphatic spread to the skeletal system is very rare. 6. The pampiniform plexus receives venous drainage from the testis, epididymis, and ductus deferens and drains into the testicular veins.

 -1  (nbme23#33)

Treat this like a VIPoma (Watery diarrhea, achlorhydria = reduced HCl in the lumen, & hypokalemia)

this will lead to metabolic acidosis d/t loss of bicarb in stool

btl_nyc  Chloride is increased though.
maxillarythirdmolar  This comment is gold. @btl_nyc, this is actually accute. you would expect hyperchloremia https://www.ncbi.nlm.nih.gov/books/NBK507698/

 +2  (nbme23#50)

Blood flow in series increases the resistance; blood flow in parallel decreases the resistance (TPR).

By blocking the umbilical veins you have in respect limited the excess flood flow to the placenta.

This reduces the flow in parallel circulation; thus increases the TPR. (MAP = cardiac out put times TPR)

This is because the total cross sectional area is reduced.

From this, there is an increased pressure in the fetal circulation.

The baroreceptors located immediately distal to the bifurcation of the common carotid artery would sense a high pressure and increase their afferent signal via CN9.

This Reduces the sympathetics and increases the parasympathetics via CN10 (vagus).

Thus, reducing the heart rate!

usmleuser007  correction: meant to say umbilical arteries (2 of them from the fetal heart to the placenta)

 +0  (nbme23#1)

The gestational sac is spherical in shape, and usually located in the upper part of the fundus of the uterus. By approximately 9 weeks of gestational age, the amniotic sac has expanded to occupy the majority of the volume of the gestational sac, eventually expanding to reduce the extraembryonic coelom to a thin layer between the amnion membrane and the mesoderm. By then, the gestational sac is usually simply called the "amniotic sac".

Development During embryogenesis, the extraembryonic coelom (or chorionic cavity) that constitutes the gestational sac is a portion of the conceptus consisting of a cavity between Heuser's membrane and the Trophoblast.

During formation of the primitive yolk sac, some of the migrating hypoblast cells differentiate into mesenchymal cells that fill the space between Heuser's membrane and the Trophoblast, forming the extraembryonic mesoderm. As development progresses, small lacunae begin to form within the extraembryonic mesoderm which enlarge to become the extraembryonic coelom.

The extraembryonic coelom divides the extraembryonic mesoderm into two layers: extraembryonic splanchnopleuric mesoderm, which lies adjacent to Heuser's membrane around the outside of the primitive yolk sac, and extraembryonic somatopleuric mesoderm, which lies adjacent to the cytotrophoblast layer of the embryo.

The chorionic cavity is enclosed by the chorionic plate, which is composed of an inner layer of somatopleuric mesoderm and an outer layer of trophoblast cells.

---WIKI


 +3  (nbme23#37)

NVM got it.

Just FYI: the CI was stated to be from 110-116 with 95% and mean of 113. So, on either there are two SD on either sides of 113 (the mean) that give the 95%.

116-113= 3 within 2SD above the mean 113-110= 3 within 2SD below the mean

3 divided by the 2 SD = 1.5 per SD.

to get from 95% to 99% you have to incorporate one more SD (3 SD) on either sides of the mean (113)

Therefore; at 99% CI 110-1.5= 108.5 CI 116+1.5= 117.5

Round these up and you get 108-118


 +0  (nbme23#45)

Aortic Diastolic Pressure

  • High TPR = high DP
  • High HR = high DP
  • High SV = high DP

Aortic Systolic Pressure

  • High Contractility = high SP
  • High SV = high SP
  • Low Compliance = high SP


 -1  (nbme23#45) 1. Aortic Diastolic Pressure 1. High TPR = high DP 2. High HR = high DP 3. High SV = high DP 2. Aortic Systolic Pressure 1. High Contractility = high SP 2. High SV = high SP 3. Low Compliance = high SP
yex  https://cvphysiology.com/Microcirculation/M012 This helps somehow, the first part about capillary pressure.
usmlelol  that's the exp part:: The average capillary hydrostatic pressure is determined by arterial and venous pressures (PA and PV), and by the ratio of post-to-precapillary resistances (RV/RA). An increase in either arterial or venous pressure will increase capillary pressure; however, a given change in PA is only about one-fifth as effective in changing PC as the same absolute change in PV. Because venous resistance is relatively low, changes in PV are readily transmitted back to the capillary, and conversely, because arterial resistance is relatively high, changes in PA are poorly transmitted downstream to the capillary.

 +1  (nbme23#42)

Like any of the COPD, the patient has a difficult time exhaling the inspired air (thus its called an obstructive disease)

COPD results in FVC decrease, FEV1/FVC ratio decrease, FRC increase, and peek expiatory flow decrease.

A tumor or any other object that would compress on or narrow these the air way tract would present as a COPD.

Inhaling and exhaling would be limited



 -2  (nbme23#38)

So as a physician per this question you will go of some neighbor's words and not confirm if the patient has an advanced directive... seems like the doc and the neighbor are in some kind of a deal here ....


 -1  (nbme23#33)

PPI side-effects: + increased risk for C. diff + Increased risk for resp infections + can cause hypomagnesia + decrease absorption of (Ca2+, Mg2+, & iron) + increased risk of osteoporotic hip fractures (d/t low serum calcium)

imnotarobotbut  That's not the right answer tho, the answer is the binding of PGE to it's receptor
tinydoc  Can someone explain to me why the PPi answer is wrong if it increases the risk of C Dif wouldnt that also cause severe diarrhea. PPIs make a lot more sense to be given to this patient in the first place.
maxillarythirdmolar  Keep it simple, stupid.
roaaaj  @tinydoc You are correct about PPI increasing the risk of C. diff, but there was no history of antibiotic use.

 -1  (nbme22#41)

This question has nothing to do with temperature (the vignette doesn't address the temperature of the water - so don't assume)

This is how you get the answer:

1) Being in outer-space or in a swimming pool up to the neck will:

a. Increases Central blood volume (more blood returns to the right side of heart = increased preload)

b. Increases ANP = increased dilation of ventricles ~ compensatory mechanism to reduce volume overload

c. Decreased ADH & Renin-aldo-system = body is in state of volume overload & needs to reduce systemic volume

usmleuser007  correction: yea it does address the water temp but the main take away is increased preload

 +1  (nbme22#45)

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

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

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

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

 +3  (nbme22#34)

1) Superficial (first-degree) = Epidermis ~ presents as red skin without blisters

2) Superficial partial thickness (second-degree) = Extends into superficial (papillary) dermis ~ Presents with redness with clear blister & blanches with pressure

3) Deep partial thickness (second-degree) = Extends into deep (reticular) dermis ~ presents as yellow or white skin with less blanching. May be blistering.

4) Full thickness (third-degree) = Extends through entire dermis ~ presents as stiff and white/brown skin. No blanching.

5) Fourth-degree = Extends through entire skin, and into underlying fat, muscle and bone ~ presents as black skin; charred with eschar

endochondral1  what is rhus dermis?
endochondral1  nvm its urshiol
btl_nyc  Allergic contact dermatitis because of contact with poison ivy.

 +0  (nbme22#29)

Intussusception is generally caused by a blockage in the GI tract caused by a tumor, polyp, diverticulum, or just immobility at part of the tract.

1) My thought was that the patient had a Meckel diverticulum yes it happens in 2 feet from the ileocecal valve; but that is in about %2 of the population

hpsbwz  Meckel diverticulum itself occurs in 2% of the population. Also it would present much sooner rather than in a 28 year old man.

 +1  (nbme22#21)

1) ADPKD = polycystins (PC2)

2) ARPKD = fibrocystin /polyductin (FPC) -- similar to polycystins

FPC protein is found on the primary cilia of epithelia cells of cortical and medullary collecting ducts and cholangiocytes of bile ducts

FPC interacts with ADPKD protein PC2 and may also participate in this regulation pathway of the mechanosensory function of the primary cilia, calcium signaling, and PCP.


 -2  (nbme22#20)

Causes

1) Avascular necrosis occurs when blood flow to a bone is interrupted or reduced. Reduced blood supply can be caused by:

2) Joint or bone trauma. An injury, such as a dislocated joint, might damage nearby blood vessels. Cancer treatments involving radiation also can weaken bone and harm blood vessels.

3) Fatty deposits in blood vessels. The fat (lipids) can block small blood vessels, reducing the blood flow that feeds bones.

4) Certain diseases. Medical conditions, such as sickle cell anemia and Gaucher's disease, also can cause diminished blood flow to bone.

For about 25 percent of people with avascular necrosis, the cause of interrupted blood flow is unknown.


 -1  (nbme22#20)

(A) Risk factors for developing avascular necrosis include:

1) Trauma = Injuries, such as hip dislocation or fracture, can damage nearby blood vessels and reduce blood flow to bones.

2) Steroid use= Use of high-dose corticosteroids, such as prednisone, is a common cause of avascular necrosis. The reason is unknown, but one hypothesis is that corticosteroids can increase lipid levels in your blood, reducing blood flow.

3) Excessive alcohol use = Consuming several alcoholic drinks a day for several years also can cause fatty deposits to form in your blood vessels.

4) Bisphosphonate use = Long-term use of medications to increase bone density might contribute to developing osteonecrosis of the jaw. This rare complication has occurred in some people treated with high doses of these medications for cancers, such as multiple myeloma and metastatic breast cancer.

5) Certain medical treatments = Radiation therapy for cancer can weaken bone. Organ transplantation, especially kidney transplant, also is associated with avascular necrosis.

(B) Medical conditions associated with avascular necrosis include:

Pancreatitis Diabetes Gaucher's disease HIV/AIDS Systemic lupus erythematosus Sickle cell anemia


 +0  (nbme22#11)

In cases of child or adult abuse

1) if there is clear evidence such as if a child states that parents punish by hitting, child is showing fear of parent ---- call child protection right away ( don't need to wait and ask)

2) same thing goes for the adult but call the adult protection services


 +0  (nbme22#36)

The process of informed consent occurs when communication between a patient and physician results in the patient’s authorization or agreement to undergo a specific medical intervention. In seeking a patient’s informed consent (or the consent of the patient’s surrogate if the patient lacks decision-making capacity or declines to participate in making decisions), physicians should:

(a) Assess the patient’s ability to understand relevant medical information and the implications of treatment alternatives and to make an independent, voluntary decision.

(b) Present relevant information accurately and sensitively, in keeping with the patient’s preferences for receiving medical information. The physician should include information about:

The diagnosis (when known) The nature and purpose of recommended interventions The burdens, risks, and expected benefits of all options, including forgoing treatment (c) Document the informed consent conversation and the patient’s (or surrogate’s) decision in the medical record in some manner. When the patient/surrogate has provided specific written consent, the consent form should be included in the record.

In emergencies, when a decision must be made urgently, the patient is not able to participate in decision making, and the patient’s surrogate is not available, physicians may initiate treatment without prior informed consent. In such situations, the physician should inform the patient/surrogate at the earliest opportunity and obtain consent for ongoing treatment in keeping with these guidelines.

AMA Principles of Medical Ethics: I, II, V, VIII


 +0  (nbme22#32)

Central nervous system regeneration

Unlike peripheral nervous system injury, injury to the central nervous system is not followed by extensive regeneration. It is limited by the inhibitory influences of the glial and extracellular environment. The hostile, non-permissive growth environment is, in part, created by the migration of myelin-associated inhibitors, astrocytes, oligodendrocytes, oligodendrocyte precursors, and microglia. The environment within the CNS, especially following trauma, counteracts the repair of myelin and neurons. Growth factors are not expressed or re-expressed; for instance, the extracellular matrix is lacking laminins. Glial scars rapidly form, and the glia actually produce factors that inhibit remyelination and axon repair; for instance, NOGO and NI-35.The axons themselves also lose the potential for growth with age, due to a decrease in GAP43 expression, among others.

usmleuser007  (wiki)

 +0  (nbme22#32)

Neuroregeneration in the peripheral nervous system (PNS) occurs to a significant degree.[5][6] After an injury to the axon, peripheral neurons activate a variety of signaling pathways which turn on pro-growth genes, leading to reformation of a functional growth cone and regeneration. The growth of these axons is also governed by chemotactic factors secreted from Schwann cells. Injury to the peripheral nervous system immediately elicits the migration of phagocytes, Schwann cells, and macrophages to the lesion site in order to clear away debris such as damaged tissue which is inhibitory to regeneration. When a nerve axon is severed, the end still attached to the cell body is labeled the proximal segment, while the other end is called the distal segment. After injury, the proximal end swells and experiences some retrograde degeneration, but once the debris is cleared, it begins to sprout axons and the presence of growth cones can be detected. The proximal axons are able to regrow as long as the cell body is intact, and they have made contact with the Schwann cells in the endoneurial channel or tube. Human axon growth rates can reach 2 mm/day in small nerves and 5 mm/day in large nerves.[4] The distal segment, however, experiences Wallerian degeneration within hours of the injury; the axons and myelin degenerate, but the endoneurium remains. In the later stages of regeneration the remaining endoneurial tube directs axon growth back to the correct targets. During Wallerian degeneration, Schwann cells grow in ordered columns along the endoneurial tube, creating a band of Büngner (boB) that protects and preserves the endoneurial channel. Also, macrophages and Schwann cells release neurotrophic factors that enhance re-growth.

(wiki)


 +2  (nbme22#2)

Two major mechanisms of action have been elucidated:

1) Flucytosine is intrafungally converted into the cytostatic fluorouracil which undergoes further steps of activation and finally interacts as 5-fluorouridinetriphosphate with RNA biosynthesis thus disturbing the building of certain essential proteins.

2) Flucytosine also undergoes conversion into 5-fluorodeoxyuridinemonophosphate which inhibits fungal DNA synthesis.

3) Thymidylate synthetase is an enzyme that catalyzes the conversion of deoxyuridine monophosphate (dUMP) to deoxythymidine monophosphate (dTMP).

Thymidine is one of the nucleotides in DNA.

With inhibition of TS, an imbalance of deoxynucleotides and increased levels of dUMP arise. Both cause DNA damage.

(WIKI)

link981  Just look at page 36 of FA 2018 and memorize that shitty diagram o De novo pyrimidine and purine synthesis they ask so much about. No need for scientific explanations for this one unless you like to waste time.

 +3  (nbme22#23)

Arthropod infections

a. Trypansoma cruzi = reduviid bug

b. Trypanosoma brucei = Tsetse fly

c. Malaria = Anopheles mosquito

d. Flavivirus Group (West Nile Virus, Dengue) = Aedes mosquito

e. Microfilariae = black fly

f. Leishmania braziliensis = sand fly

g. Borrelia & Babesia =Ixodes tick

h. Rickebsia rickebsii & Francisella tularensis = Dermacentor tick

i. Rikebsia prowazekii = lice

j. Loa loa (African eye worm) = deer fly

k. Wuchereria bancrofti = mosquitoes


 +0  (nbme22#23) 16. Arthropod infections a. Trypansoma cruzi = reduviid bug b. Trypanosoma brucei = Tsetse fly c. Malaria = Anopheles mosquito d. Flavivirus Group (West Nile Virus, Dengue) = Aedes mosquito e. Microfilariae = black fly f. Leishmania braziliensis = sand fly g. Borrelia & Babesia =Ixodes tick h. Rickebsia rickebsii & Francisella tularensis = Dermacentor tick i. Rikebsia prowazekii = lice j. Loa loa (African eye worm) = deer fly k. Wuchereria bancrofti = mosquitoes


 +1  (nbme22#15)

Per Pathoma:

Most common in postmenopausal women:

1) fibrocystic changes, intraductal papilloma, Fibroadenoma

More likely in postmenopausal women: 1) phyllodes tumor (fibroadenoma-like tumor) 2) Breast cancers increased risk d/t 1) increased age, duration of estrogen throughout life (early menarche, late menopause, obesity) 2) Atypical hyperplasia 3) First degree relatives

Question states presents it as: a) 2cm firm, nontender mass b) no axillary lymphadenopathy or nipple discharge c) extremly radiodense mass with irregular margins clustered irregular microcalcifications

so what can it be: 1) DICS = does not usually produce mass

2) Comedo type = high- grade cells with necrosis & dystrophic calcifications at center of duct

3) Paget Disease = involves the skin of the nipple (underlying carcinoma)

4) IDC = a) forms duct-like structures (>80% of cases) b) mass detected by physical examination (check) c) usually 1cm or greater (check) d) Desmoplastic stroma = connective tissue growing with tumor (supports tumor) ~~~ (check -- irregular margins) e) Medullary Carcinome (IDC) = mimics fibroadenoma

5) LCIS & ILC = DO NOT produce calcifications or mass a) ILC - cells have "single-file pattern" think of a beaded necklace and you cut it in middle (lack E-cadherin)

usmleuser007  correction Most common in premenopausal women: 1) fibrocystic changes, intraductal papilloma, Fibroadenoma

 +2  (nbme22#16)

Mother is Rh-neg --> she will generate RH-antibodies 1) fetus affected by Anti-Rh if it is Rh-positive 2) even if O-Rh-Positive is given, then still mother's Rh-antibodies will attack transfused blood due to its cells containing Rh+ 3) therefore, O-Rh-negative is best


 -5  (nbme22#48)

Note: the questions stated "respiratory burst" suggesting an URT infection.

1) this rules out anything but respiratory infection (non rep infection: E. coli, E. faceium)

2) G6PD deficiency more susceptible to catalase positive organisms -- this rules out (all strep organisms)

3) Left with H. influenzae & Straph. aureus (BOTH are catalase positive)

4) Encapsulated organism are most concerning when there is asplenia.

imnotarobotbut  Respiratory burst has nothing to do with a respiratory infection. It describes the process of phagocytosing a bacteria and using NADPH oxidase/ROS to lyse it
belleng  Aspergillus is still in the running, it is catalase positive as well...but not a choice

 +0  (nbme22#7)

Someone care to explain why [time to steady-state concentration] is not the correct answer?

omerta  In pharmacokinetics, steady state refers to the situation where the overall intake of a drug is fairly in dynamic equilibrium with its elimination. In practice, it is generally considered that steady state is reached when a time of 4 to 5 times the half-life for a drug after regular dosing is started. The time to reach steady state is defined by the elimination half-life of the drug. So in a patient with renal dysfunction, the plasma half-life is going to be prolonged and the time to reach steady state will increase proportionally.
belleng  loading dose is independent of the concentration of the drug in the plasma and the dose frequency...this is why you give a patient who is seizing a huge dose of anti-seizure meds in order to reach a theraputic range on the first dose despite the high risk of toxicity and side effects...primary objective when seizing is stoping the seizure so you want to increase the dose response curve with a massive load
belleng  loading dose is independent of DOSE (should have said dose, not concentration in plasma) & FREQUENCY

 +1  (nbme22#9)

Actinin is a microfilament protein. α-Actinin is necessary for the attachment of actin filaments to the Z-lines in skeletal muscle cells,[1] and to the dense bodies in smooth muscle cells.[2] The functional protein is an anti-parallel dimer, which cross-links the thin filaments in adjacent sarcomeres, and therefore coordinates contractions between sarcomeres in the horizontal axis.

The non-sarcomeric α-actinins, encoded by ACTN1 and ACTN4, are widely expressed. ACTN2 expression is found in both cardiac and skeletal muscle, whereas ACTN3 is limited to the latter. Both ends of the rod-shaped α-actinin dimer contain actin-binding domains.

Mutations in ACTN4 can cause the kidney disease focal segmental glomerulosclerosis (FSGS).

(WIKI)


 +5  (nbme22#45)

my list of spindle type cells and conditions:

  • a. NF-1
  • b. NF-2 ~ Schwannoma (Antoni A) = Cutaneous neurofibroma ~ high cellularity (w/ palisading patterns with interspersing nuclear-free zones called Verocay bodies
  • c. Leiomyoma (uterus & esophagus)
  • d. Mesothelioma (cytokeratin positive)
  • e. Anaplastic Thyroid cancer (biphasic & along with giant cells)
  • f. Medullary Thyroid cancer (can also have polygonal cells)
  • g. Primary cardiac angiosarcoma (malignant vascular spindle cells)
  • h. Osteosarcoma (bone cancer) (pleomorphic cells)
  • i. Meningioma
  • j. Kaposi's Sarcoma (HHV-8) = Slit-like vascular spaces with plump spindle-shaped stromal cells
drdoom  @usmleuser007 to make lists display correctly, try using the plus sign (+) for each "bullet point"; that should work
mcl  I love this and I love you
usmleuser007  LOL thanks, had to ddo a lot of digging since "spindle cells" are commonly tested

 +0  (nbme22#22)

1) Analysis of variance is a procedure used for comparing sample means to see if there is sufficient evidence to infer that the means of the corresponding population distributions also differ.

2) Where t-test compare only two distributions, analysis of variance is able to compare many. • What does the one-way part mean? It is one dependent variable (always continuous) and exactly one independent variable (always categorical). A single independent variable can have many levels.



 +10  (nbme22#22)

Just remember:

1) T-test (tea for two) = looks at the mean values of 2 groups

2) ANOVA (analysis of variance) ~ like t-test but = looks at mean values of 3 or more groups

3) Chi-square = looks at the (%) or proportions between 2 or more groups.

so, just look for how many groups being addressed and what values they are using (% or means)


 +5  (nbme22#17)

1) EBV = Burkitt lymphoma, Hodgkin lymphoma, nasopharyngeal carcinoma, 1° CNS lymphoma (in immunocompromised patients)

2) HBV & HCV = Hepatocellular carcinoma

3)HHV-8 = Kaposi sarcoma

4) HPV= Cervical and penile/anal carcinoma (types 16, 18), head and neck cancer

5) H. pylori = Gastric adenocarcinoma and MALT lymphoma

6) HTLV-1 = Adult T-cell leukemia/lymphoma

7) Liver fluke (Clonorchis sinensis) = Cholangiocarcinoma

8) Schistosoma haematobium = Bladder cancer (squamous cell)

some0217710  Aren’t both H.pylori and EBV associated with gastric lymphoma?

 +0  (nbme22#35)

1) label D (VLDL -->ILD --> LDL) = anything that increased LPL = Fibrates which use PPAR-alpha (Rx) are good at reducing [VLDL]; therefore, less VLDL means more ILD.

2) VLDL --> fatty acid oxidation = using fats (TAGs) for energy production Here PPAR-gamma plays a role= which are Thiazolidinediones (also called glitazones) are a class of medicines that may be used for the treatment of type 2 diabetes. They are also good at reducing serum TAGs

Note VLDL are very rich in TAGs


 +2  (nbme22#31)

Just note why other answers are not correct:

  1. Egophony is an increased resonance of voice sounds heard when auscultating the lungs, often caused by lung consolidation and fibrosis.

    • a. It is due to enhanced transmission of high-frequency sound across fluid, such as in abnormal lung tissue, with lower frequencies filtered out.
  2. Whispered pectoriloquy refers to an increased loudness of whispering noted during auscultation with a stethoscope on the lung fields on a patient’s torso.

    • a. Usually spoken sounds of a whispered volume by the patient would not be heard by the clinician auscultating a lung field with a stethoscope.

    • b. However, in areas of the lung where there is lung consolidation, these whispered spoken sounds by the patient (such as saying ‘ninety-nine’) will be clearly heard through the stethoscope.

    • c. This increase in sound exists because sound travels faster and thus with lower loss of intensity through liquid or solid (“fluid mass” or “solid mass,” respectively, in the lung) versus gaseous (air in the lung) media.

    • d. Whispered pectoriloquy is a clinical test typically performed during a medical physical examination to evaluate for the presence of lung consolidation, which could be caused by cancer (solid mass) or pneumonia (fluid mass).

titanesxvi  why not wheezing?

 +4  (nbme21#2)

1) Very important to note that Tay-Sachs disease has more sensitive startle (moro) reflex in neonates with increased head circumference.

2) Fabry disease = tend to have audio-visual defects w/o liver involvement

3) Niemann-pick disease = anemia & hypotonia with areflexia


 +0  (nbme21#4)

Serine phosphorylation will reduce insulin's affects. It acts on teh tyrosine kinase.


 +1  (nbme21#17)

Confidence interval increases with decreased sample size.

usmleuser007  would require a a large sample size to see if there is a true difference
claptain  This question is bogus. CI does not always increase with decreased sample size or vice versa. Four readings with small variation would give a narrower CI than 10 readings with greater variation. The only thing you can be certain about by adding more samples is that the CI will most likely change, but which direction is uncertain.
bartolomoose  Recall the formula for 95%ci Mean +/- 1.96* (SD/sqrt(samplesize))

 +5  (nbme21#40)
1. Example of inaccurate but highly precise 
    a. 500 patients seeing a particular doctor for a particular illness
2. Example of accurate but imprecise
    a. 10 patients undergo a screening at a mall 
3. Both Accurate and precise 
    a. 500 patients (high precision) undergo a screening (high accuracy ~ no bias or systemic error)

 +2  (nbme21#7)

Inhaled glue is more likely than alcohol b/c of its ease of access for a minor and relative abuse potential in the age group.


 +8  (nbme21#43)
  1. Hemostasis (blood clotting): Within the first few minutes of injury,
    1. platelets in the blood begin to stick to the injured site.
    2. This activates the platelets, causing a few things to happen.
    3. They change into an amorphous shape, more suitable for clotting, and they release chemical signals to promote clotting.
    4. This results in the activation of fibrin, which forms a mesh and acts as "glue" to bind platelets to each other.
    5. This makes a clot that serves to plug the break in the blood vessel, slowing/preventing further bleeding.[5][6]

  2. Inflammation: During this phase, damaged and dead cells are cleared out, along with bacteria and other pathogens or debris.
    1. This happens through the process of phagocytosis, where white blood cells "eat" debris by engulfing it. 
    2. Platelet-derived growth factors are released into the wound that cause the migration and division of cells during the proliferative phase.

  3. Proliferation (growth of new tissue): In this phase, angiogenesis, collagen deposition, granulation tissue formation, epithelialization, and wound contraction occur.
    1. In angiogenesis, vascular endothelial cells form new blood vessels.
    2. In fibroplasia and granulation tissue formation, fibroblasts grow and form a new, provisional extracellular matrix (ECM) by excreting collagen and fibronectin.
    3. Concurrently, re-epithelialization of the epidermis occurs, in which epithelial cells proliferate and 'crawl' atop the wound bed, providing cover for the new tissue.
    4. In wound contraction, myofibroblasts decrease the size of the wound by gripping the wound edges and contracting using a mechanism that resembles that in smooth muscle cells.
    5. When the cells' roles are close to complete, unneeded cells undergo apoptosis.
  4. Maturation (remodeling): During maturation and remodeling,

    1. collagen is realigned along tension lines, and cells that are no longer needed are removed by programmed cell death, or apoptosis.

  5. Approximate times of the different phases of wound healing,[10] with faded intervals marking substantial variation, depending mainly on wound size and healing conditions, but image does not include major impairments that cause chronic wounds.

 +1  (nbme21#36)

Chondrosarcoma = mainly affects the axial skeleton than the appendicular skeleton

Enchondroma = mainly affects the hands and feet; are cyst like


 +2  (nbme21#12)

Can someone please explain why can't alcohol be correct in this setting?

niboonsh  rhinorrhea is specific to withdrawal from opioids (aka heroin). Look at page 554 in FA2018
dr_jan_itor  what if the alcoholic just has a concurrent rhinovirus infection ;)

 +3  (nbme21#17)

essential Amino acids (AA)

1) Adults require 9 (AA) = able to make argnine via urea cycle 2) Children require 10 (AA) = they are still developing 3) With PKU tyrosine becomes essential in both adults and children


 +1  (nbme21#24)

As per FA 1) fatty infiltration 2) cellular ballooning 3) eventual necrosis

hyperfukus  thanks u saved me time in looking that up :)

 +2  (nbme21#17)
1. "Three HAL fans will try meth"
    a. Threonine = Three 
    b. Histidine; Arginine; Lysine = HAL
    c. Phenylalanine = fans
    d. Valine; Isoleucine; Leucine = will
    e. Tryptophan = try
    f. Methionine = meth
pparalpha  Thanks! Good mnemonic

 +5  (nbme21#17)

If you couldn't remember which were essential; then alternative would have been to realize that growing children need cells to divide. This requires DNA replication and translation. Of which the nucleic acid thyime is important. It requires a methyl transfer.

This is where methionine comes in. Methionine combines with ATP to form SAM (a methyl donor)

whossayin  That’s a legendary explanation. Thanks dude!

 +2  (nbme21#32)

Ifall else fails: note that other answer choices are COPD types

dragon3  (except sarcoidosis)

 +0  (nbme21#37)

Remember 1) competitive inhibitors ~ lines Cross at y-intersect 2) Non-competitive inhibitors ~ no line cross


 +0  (nbme21#9)

CNS Hemorrhage/ damage 1) 12-48 Hrs = red neurons 2) 1-3 days = neutrophils (liquefactive necrosis) 3) 3-5 = macrophages (microglia) 4) 1-2 weeks = Reacitve gliosis (+ vascular proliferation) 5) more than 2 weeks = Glial scar

(note: the pathogenesis is similar to MI and its scar formation; however, the time course for CNS is just faster)


 +0  (nbme21#12)

For RCC: (As per UWORLD)

Symmetric bilateral lower extremity pitting edema and tortuous abdominal veins are concerning for an inferior vena cava (IVC) obstruction, which, in the setting of a left-sided flank mass, suggests renal cell carcinoma (RCC) with extension into the IVC.  RCC accounts for >90% of all malignancies arising in the kidney and is highly associated with smoking.  Patients with RCC classically have a triad of flank pain, palpable mass, and hematuria, although many remain asymptomatic until the disease is advanced. RCC is a highly vascular tumor that invades the renal vein in up to 25% of cases.  IVC obstruction can occur due to intraluminal extension and thrombus formation, rather than mass effect from the tumor itself. 

The obstruction can occur acutely or gradually over time.  In chronic cases, collateral venous circulation may develop based on the site of the obstruction.  Prominent abdominal wall collateral veins, as in this patient, suggest obstruction of the upper segment of the IVC.

nor16  high blood pressure, i.e. Hypertension, risk factors for atheroscl., bruit !!! over left abdomen, secondary art. Hypertension. they always want the renal artery stenosis (like vWF in coag. disorders...)

 +0  (nbme21#12)

Just realized that renal cell carcinoma isn't the correct answer b/c it invaded the venous circulation and not the arterial. BP may not be affected as much. if RCC were the answer then then there would have been edema present and/or renal HTN.

sympathetikey  Also, just thinking out loud, in the case of RCC, it's the kidney tissue that's dysplastic & moving, so technically the renal artery itself isn't dysplastic, right?

 +1  (nbme21#35)

CO is increased with 1) decreased afterload 2) increased preload 3) Increased contractility

An ateriovenous fistula creates an alternative route for atrial blood into the venous circulation w/o going past the arterioles (the major cause of resistance). Thus, by doing so the TPR (afterload) decreases and the CO is increased.


 +0  (nbme21#46)

https://www.mayoclinic.org/diseases-conditions/precocious-puberty/symptoms-causes/syc-20351811

Symptoms Precocious puberty signs and symptoms include development of the following before age 8 in girls and before age 9 in boys.

Breast growth and first period in girls Enlarged testicles and penis, facial hair and deepening voice in boys Pubic or underarm hair Rapid growth Acne Adult body odor


 +0  (nbme21#13)

just a hunch.... Omeprazole is always the right answer

nala_ula  Famotidine is an H2 blocker which really only stops acid secretion via the stimulation of H+/K+ ATPase by histamine, but it still has vagus and gastrin stimulation. If you use Omeprazole, you get irreversible inhibition of the pump itself which stops the secretion of acid even if there is histamine, gastrin, vagus stimulation.
temmy  what about the healing of her mucosa. Is that not the action of prostaglandin?. That threw me off cos according to FA, misoprostol increases secretion of the gastric mucosa
cry2mucheveryday  same doubt..marked miso
sahusema  I guess because misoprostol is more associated with treatment of NSAID related ulcers and PPIs are 1st line DOC for GERD?

 +1  (nbme21#12)

Don't this is UC or Crohns. For this question you have to have noticed the age (66 year-old). Lower left quadrant = diverticulitis of elderly & Lower right quadrant = angiodysplasia of elderly (think these were mentioned in Pathoma)


 +1  (nbme20#2)

Norovirus (Sketchy) = Affects where a lot of people are in close quarters - especially common on cruises - 90% of all diarrheal outbreaks on cruises

sbryant6  Rotavirus occurs in unvaccinated children. In order for it to spread, all those kids would have to be unvaxxed.

 +0  (nbme20#32)

To answer this question is to note that: 1) alkaline phosphatase activity is linked with osteoblasts.


 +0  (nbme20#16)

Tuberous sclerosis = "ash-leaf spots" = oval-shaped areas pale areas on skin. often d/t hamartomas


 +2  (nbme20#14)

All other types are either pigmented or have scales. -- process of elimination


 +1  (nbme20#41)

https://www.ncbi.nlm.nih.gov/pubmed/301658

Relief of intractable pain was produced in six human patients by stimulation of electrodes permanently implanted in the periventricular and periaqueductal gray matter. The level of stimulation sufficient to induce pain relief seems not to alter the acute pain threshold. Indiscriminate repetitive stimulation produced tolerance to both stimulation-produced pain relief and the analgesic action of narcotic medication; this process could be reversed by abstinence from stimulation. Stimulation-produced relief of pain was reversed by naloxone in five out of six patients. These results suggest that satisfactory alleviation of persistent pain in humans may be obtained by electronic stimulation.

usmleuser007  These questions seem unfair to test because they are based on experimental data. Guess they are there to limit a perfect score.
xxabi  I just read it as patients take opioids to blunt or control pain. So if the electrode does the same thing (decrease pain), then an antagonist of opioids (naloxone) would bring the pain back? Idk if that reasoning is sound but that's the logic I used, I didn't even think of it as experimental.
xxabi  Also its the only one that's an opioid antagonist from the list!
redvelvet  they are writing these questions in an evidence-based manner because the questions in medicine cannot be produced by a self imagination or logic. But that doesn't mean that we have to know their exact evidence like this question. we can use our own basic knowledge and adjust it with logic. so opioids have an analgesic effect in the body and naloxone can revert it.
champagnesupernova3  Anything that reduces pain by brain stimulation is increasing endogenous opiods like endorphins and encephalitis.
champagnesupernova3  Enkephalins* not encephalitis

 +2  (nbme20#16)

Salivary secretion 1. At low flow = High concentration of potassium; low concentrations of sodium, bicarb, & chloride 2. at high flow = low concentration of potassium; high concentrations of sodium, bicarb, & chloride

sherry  That's exactly what I was thinking when I was taking the test. But I was sidetracked by same HCO3 level. Can somebody explain this part to me??
charcot_bouchard  Because salivary duct removes Na & Cl while secrete K & Hco3 in lumen. In low flow rate HCO3 & K inc because duct is doing its thing for more time. At high flow rate K slightly dec (as cant be secrted as much) but HCO3 stays almost same. the reason is high flow indicates higher metabolism & higher bicarb production.
cienfuegos  Regarding the bicarb (via BRS Physiology, which explains flow rate as coming down to "contact time" where slow flow allows more reabsorption of NaCl): The only ion that does not “fit” this contact time explanation is HCO3−; HCO3− secretion is selectively stimulated when saliva secretion is stimulated.

 -1  (nbme20#37)

Vitamin E deficiency is known to cause similar spinal defects as Vitamin B12 deficiency. However, anemia is not seen.

ergogenic22  Also corticalspinal tract symptoms are not seen, but dorsal column and spinocerebellar tracts are seen
sinforslide  In this case, patient's CF also predisposes fat-soluble vitamin deficiency.
breis  FA pg 70
usmleuser007  Correction: Read more on this Vitamin-E deficiency can in fact cause anemia - hemolytic anemia. This is b/c VitE work as an anti-oxidant; and therefore with reduced anti-oxidation RBCs are more prone to oxidative injuries.




Subcomments ...

submitted by mousie(82),

if your CO falls ... wouldn't that cause vasoconstriction in the lung vasculature? hypoxia induced vasoconstriction?

ug123  My take on this----His respirations are high-22/min--that will cause c02 washout---so actually lung has high oxygen---pulmonary vasodilation. Dont know if its right. +3  
usmleuser007  My understanding is that the pulmonary circulation changes very little in terms of an acute MI. It is b/c pulmonary circulation has a lot more room to fill with blood much like the spleen in terms of blood accumulation. With higher volume of blood in pulmonary circulation, more blood vessels are able to be recruited specially the apex. With more recruited blood vessels = reduced pressure d/t circulation in parallel +  


submitted by keycompany(115),

Can somebody who understand why PVR decreases with a Left-Sided infarct please enlighten me. I would also appreciate it if you could relate it to right sided heart failure too (i.e. how would it change).

sajaqua1  I believe that keycompany's answer comes the closest. In an MI, consider it as cardiogenic shock. The heart is a pump, and it is failing to move blood out of the heart and into vasculature. This is why PCWP increases. Because of insufficient output, the body has a sympathetic response. The catecholamines then cause vasoconstriction in peripheral vasculature to keep blood pressure up and continue flow, leading to increased SVR. Meanwhile, the sympathetic response causes vasodilation in the lungs; this would be an appropriate autoregulatory response, because the body is trying to keep up the flow of oxygen throughout the system. This decreases PVR. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5715548/ Is a pretty good article on this. Of course the binding of catetcholamines changes depending on saturation and the response is not perfectly understood. +6  
usmleuser007  My understanding is that the pulmonary circulation changes very little in terms of an acute MI. It is b/c pulmonary circulation has a lot more room to fill with blood much like the spleen in terms of blood accumulation. With higher volume of blood in pulmonary circulation, more blood vessels are able to be recruited specially the apex. With more recruited blood vessels = reduced pressure d/t circulation in parallel. +  


lsmarshall  Rectal prolapse through posterior vagina ("rectocele"). https://www.drugs.com/cg/images/en2362586.jpg +5  
famylife  "When a rectocele becomes large, stool can become trapped within it, making it difficult to have a bowel movement or creating a sensation of incomplete evacuation. Symptoms are usually due to stool trapping, difficulty passing stool, and protrusion of the back of the vagina through the vaginal opening. During bowel movements, women with large, symptomatic rectoceles may describe the need to put their fingers into their vagina and push back toward the rectum to allow the stool to pass (“splinting”). Rectoceles are more common in women who have delivered children vaginally." https://www.fascrs.org/patients/disease-condition/pelvic-floor-dysfunction-expanded-version +5  
usmleuser007  really like the pubic hair.... +  


submitted by m-ice(122),

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? +  


submitted by m-ice(122),

The "likelihood of missing an association" refers to Type II error. The risk of Type II error is represented by beta. This could be confused with power, which is 1 - beta.

usmleuser007  Just rereading this question without the stress, i got it quickly! Could't believe i missed something as simple as this. +1  


submitted by neonem(251),

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 ? +  


submitted by mousie(82),

Why no sweating? I mean I get Ecstasy is probably the drug of choice before an all night dance party (lol) but don't understand why there would be cold extremities and no sweating when is FA it says hyperthermia and rhabdo????

sympathetikey  FA says, "euphoria, disinhibition, hyperactivity, distorted sensory and time perception, bruxism. Lifethreatening effects include hypertension, tachycardia, hyperthermia, hyponatremia, serotonin syndrome." So I think they wanted you to see Sinus Tachy and jump for MDMA. Idk why Ketamine couldn't also potentially be correct though. +1  
amorah  I picked ketamine because it said no diaphoresis. But if you need to find a reason, I guess the half life of ketamine might rule it out. Remember from sketchy, ketamine is used for anaesthesia induction, so probably won't keep the HR and BP high for 8 hrs. In fact, its action is ~10-15 mins-ish iv. +2  
yotsubato  Because the NBME is full of fuckers. The guy is probably dehydrated so he cant sweat anymore? +1  
fulminant_life  you wouldnt see tachycardia with ketamine. It causes cardiovascular depression but honestly i saw " all-night dance party" picked the mdma answer and moved on lol +3  
monkd  Ketamine acts as a sympathomimetic but oh well. NBME hasn't caught on to ketamine as a drug of recreation :) +  
usmleuser007  Why not LSD? +  
d_holles  @usmleuser007 LSD doesn't cause HTN and ↑ HR. +  
sbryant6  @fulminant_life FALSE. KETAMINE CAUSES CARDIOVASCULAR STIMULATION. +1  
dashou19  Take a look at why the patient has pale and cold extremities. "Mechanistic clinical studies indicate that the MDMA-induced elevations in body temperature in humans partially depend on the MDMA-induced release of norepinephrine and involve enhanced metabolic heat generation and cutaneous vasoconstriction, resulting in impaired heat dissipation." https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5008716/ +  


submitted by usmleuser007(110),

Blood flow in series increases the resistance; blood flow in parallel decreases the resistance (TPR).

By blocking the umbilical veins you have in respect limited the excess flood flow to the placenta.

This reduces the flow in parallel circulation; thus increases the TPR. (MAP = cardiac out put times TPR)

This is because the total cross sectional area is reduced.

From this, there is an increased pressure in the fetal circulation.

The baroreceptors located immediately distal to the bifurcation of the common carotid artery would sense a high pressure and increase their afferent signal via CN9.

This Reduces the sympathetics and increases the parasympathetics via CN10 (vagus).

Thus, reducing the heart rate!

usmleuser007  correction: meant to say umbilical arteries (2 of them from the fetal heart to the placenta) +  


submitted by hayayah(394),

Carbonic anhydrase inhibitors (eg, acetazolamide) and loop diuretics (eg, furosemide) are thought to exert their effect on ICP by reducing cerebrospinal fluid (CSF) production at the choroid plexus.

Google says mechanism is unknown LOL.

usmleuser007  Just FYI: Mannitol can also be used to reduce ICP by drawing free water out of CNS Howeveer, it can cause hypernatremia, pulmonary edema, and expansion of ECV can exacerbate heart failure +  


submitted by sajaqua1(198),

A standard deviation is a measure of probability in resembling the average. One standard deviation on a bell curve distribution creates a 67% chance that the answer will lie in there. Two standard deviations will create a 95% chance. Three standard deviations creates a 99.7% chance.

This patient has an average of 113, and a 95% confidence at 110-116 means that the SD is 1.5 . So one additional SD would give us a range of 108.5-117.5, rounded to 108-118.

usmleuser007  How did you get the SD to be 1.5? +  
usmleuser007  NVM Got it +  


submitted by sajaqua1(198),

A standard deviation is a measure of probability in resembling the average. One standard deviation on a bell curve distribution creates a 67% chance that the answer will lie in there. Two standard deviations will create a 95% chance. Three standard deviations creates a 99.7% chance.

This patient has an average of 113, and a 95% confidence at 110-116 means that the SD is 1.5 . So one additional SD would give us a range of 108.5-117.5, rounded to 108-118.

usmleuser007  How did you get the SD to be 1.5? +  
usmleuser007  NVM Got it +  


Patient has a ganglion cyst, which can spontaneously regress.

medschul  Mine would beg to differ >:O +1  
usmleuser007  Where would I have come across something like this (FA, Pathoma, or out of my S)? +1  


submitted by dubchak7(0),

They suggest Misoprostol to counteract NSAIDs... Why not PPIs?

hayayah  PPI's don't have many side effects! If the question didn't involve the diarrhea side effect the answer would have been to give her a PPI. +  
tsarcoidosis  I guess one takeaway is that PPIs don't directly cause diarrhea, but they do increase the risk for C-diff, which causes diarrhea. +2  
usmleuser007  PPI side-effects: + increased risk for C. diff + Increased risk for resp infections + can cause hypomagnesia + decrease absorption of (Ca2+, Mg2+, & iron) + increased risk of osteoporotic hip fractures (d/t low serum calcium) +  
temmy  The patient got severe gastric burning and discomfort as an effect of the drug. My logic was since the patient was taking an NSAID it had to be a COX 1 inhibitor that destroys the protective barrier of the GI mucosa due to inhibition of prostaglandin so we needed to treat with a drug that will regenerate prostaglandin and prostaglandin is a vasodilation which might be the reason for the diarrhea. +  


submitted by usmleuser007(110),

my list of spindle type cells and conditions:

  • a. NF-1
  • b. NF-2 ~ Schwannoma (Antoni A) = Cutaneous neurofibroma ~ high cellularity (w/ palisading patterns with interspersing nuclear-free zones called Verocay bodies
  • c. Leiomyoma (uterus & esophagus)
  • d. Mesothelioma (cytokeratin positive)
  • e. Anaplastic Thyroid cancer (biphasic & along with giant cells)
  • f. Medullary Thyroid cancer (can also have polygonal cells)
  • g. Primary cardiac angiosarcoma (malignant vascular spindle cells)
  • h. Osteosarcoma (bone cancer) (pleomorphic cells)
  • i. Meningioma
  • j. Kaposi's Sarcoma (HHV-8) = Slit-like vascular spaces with plump spindle-shaped stromal cells
drdoom  @usmleuser007 to make lists display correctly, try using the plus sign (+) for each "bullet point"; that should work +  
mcl  I love this and I love you +1  
usmleuser007  LOL thanks, had to ddo a lot of digging since "spindle cells" are commonly tested +  


submitted by usmleuser007(110),

This question has nothing to do with temperature (the vignette doesn't address the temperature of the water - so don't assume)

This is how you get the answer:

1) Being in outer-space or in a swimming pool up to the neck will:

a. Increases Central blood volume (more blood returns to the right side of heart = increased preload)

b. Increases ANP = increased dilation of ventricles ~ compensatory mechanism to reduce volume overload

c. Decreased ADH & Renin-aldo-system = body is in state of volume overload & needs to reduce systemic volume

usmleuser007  correction: yea it does address the water temp but the main take away is increased preload +  


submitted by dr.xx(39),

The most common and severe form of autosomal dominant polycystic kidney disease (ADPKD) results from mutations in PKD1, encoding polycystin-1 (PC1)..

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4348948/

yotsubato  Here we thank FA for failing us yet again. Giving us PKD1, but not polycystin. I got the question right but I just guessed it because nothing else made sense. +3  
usmleuser007  Autosomal dominant polycystic kidney disease 1) occurs in patients with mutations in the gene (PKD1) encoding polycystin-1 (PC1). 2) PC1 is a complex polytopic membrane protein expressed in cilia that undergoes autoproteolytic cleavage at a G protein–coupled receptor proteolytic site (GPS). 3) A quarter of PKD1 mutations are missense variants, though it is not clear how these mutations promote disease. 4) GPS cleavage is required for PC1 trafficking to cilia. 5) A common feature among a subset of pathogenic missense mutations is a resulting failure of PC1 to traffic to cilia regardless of GPS cleavage. 6) Missense mutation in the gene encoding polycystin-2 (PC2) that prevented this protein from properly trafficking to cilia.  +1  


submitted by usmleuser007(110),

(A) Risk factors for developing avascular necrosis include:

1) Trauma = Injuries, such as hip dislocation or fracture, can damage nearby blood vessels and reduce blood flow to bones.

2) Steroid use= Use of high-dose corticosteroids, such as prednisone, is a common cause of avascular necrosis. The reason is unknown, but one hypothesis is that corticosteroids can increase lipid levels in your blood, reducing blood flow.

3) Excessive alcohol use = Consuming several alcoholic drinks a day for several years also can cause fatty deposits to form in your blood vessels.

4) Bisphosphonate use = Long-term use of medications to increase bone density might contribute to developing osteonecrosis of the jaw. This rare complication has occurred in some people treated with high doses of these medications for cancers, such as multiple myeloma and metastatic breast cancer.

5) Certain medical treatments = Radiation therapy for cancer can weaken bone. Organ transplantation, especially kidney transplant, also is associated with avascular necrosis.

(B) Medical conditions associated with avascular necrosis include:

Pancreatitis Diabetes Gaucher's disease HIV/AIDS Systemic lupus erythematosus Sickle cell anemia



submitted by usmleuser007(110),

Central nervous system regeneration

Unlike peripheral nervous system injury, injury to the central nervous system is not followed by extensive regeneration. It is limited by the inhibitory influences of the glial and extracellular environment. The hostile, non-permissive growth environment is, in part, created by the migration of myelin-associated inhibitors, astrocytes, oligodendrocytes, oligodendrocyte precursors, and microglia. The environment within the CNS, especially following trauma, counteracts the repair of myelin and neurons. Growth factors are not expressed or re-expressed; for instance, the extracellular matrix is lacking laminins. Glial scars rapidly form, and the glia actually produce factors that inhibit remyelination and axon repair; for instance, NOGO and NI-35.The axons themselves also lose the potential for growth with age, due to a decrease in GAP43 expression, among others.

usmleuser007  (wiki) +  


submitted by usmleuser007(110),

Per Pathoma:

Most common in postmenopausal women:

1) fibrocystic changes, intraductal papilloma, Fibroadenoma

More likely in postmenopausal women: 1) phyllodes tumor (fibroadenoma-like tumor) 2) Breast cancers increased risk d/t 1) increased age, duration of estrogen throughout life (early menarche, late menopause, obesity) 2) Atypical hyperplasia 3) First degree relatives

Question states presents it as: a) 2cm firm, nontender mass b) no axillary lymphadenopathy or nipple discharge c) extremly radiodense mass with irregular margins clustered irregular microcalcifications

so what can it be: 1) DICS = does not usually produce mass

2) Comedo type = high- grade cells with necrosis & dystrophic calcifications at center of duct

3) Paget Disease = involves the skin of the nipple (underlying carcinoma)

4) IDC = a) forms duct-like structures (>80% of cases) b) mass detected by physical examination (check) c) usually 1cm or greater (check) d) Desmoplastic stroma = connective tissue growing with tumor (supports tumor) ~~~ (check -- irregular margins) e) Medullary Carcinome (IDC) = mimics fibroadenoma

5) LCIS & ILC = DO NOT produce calcifications or mass a) ILC - cells have "single-file pattern" think of a beaded necklace and you cut it in middle (lack E-cadherin)

usmleuser007  correction Most common in premenopausal women: 1) fibrocystic changes, intraductal papilloma, Fibroadenoma +  


submitted by mcl(202),

To expand on this, pathologyoutlines describes the histology of kapowsi sarcoma as "spindle cells forming slits with extravasated red blood cells"

mcl  lul i don't know why i spell kaposi like that, my b +1  
bubbles  This site is super helpful. Thanks for sharing :) +  
mcl  yesssssss ofc <3 I love path outlines +  
usmleuser007  Just realize that spindle cells are similar to the endothelial cells of blood vessels. Anything that have vessel association might have spindle-shaped cells. a. NF-1 b. NF-2 ~ Schwannoma (Antoni A) = Cutaneous neurofibroma ~ high cellularity (w/ palisading patterns with interspersing nuclear-free zones called Verocay bodies c. Leiomyoma (uterus & esophagus) d. Mesothelioma (cytokeratin positive) e. Anaplastic Thyroid cancer (biphasic & along with giant cells) f. Medullary Thyroid cancer (can also have polygonal cells) g. Primary cardiac angiosarcoma (malignant vascular spindle cells) h. Osteosarcoma (bone cancer) (pleomorphic cells) i. Meningioma j. Kaposi's Sarcoma (HHV-8) = Slit-like vascular spaces with plump spindle-shaped stromal cells +1  


submitted by mcl(202),

Despite a numeric value (blood pressure) being measured, patients would be designated either hypertensive or normotensive. To my understanding, the best test for comparing categorical variables across groups is a chi square test.

In contrast, a t-test is used to compare between the means of two groups (measured variable must be quantitative).



submitted by mcl(202),

page 119 FA Patient is presenting months after the transplant, which means it can't be hyperacute unless he stopped taking his immunosuppressants. Acute/chronic/GVH disease are mediated by T cells for the most part (I think), so this would mean lymphocytic infiltrates.

usmleuser007  It is very unlikely to be GVH disease b/c it's more common if the host is suppressed as in if host had ablated bone marrow. (FA states that it's more common with bone marrow & liver transplants) +1  
usmleuser007  any one care to explain why fibrous scars with plasma cells not a good option?... +1  


submitted by mcl(202),

page 119 FA Patient is presenting months after the transplant, which means it can't be hyperacute unless he stopped taking his immunosuppressants. Acute/chronic/GVH disease are mediated by T cells for the most part (I think), so this would mean lymphocytic infiltrates.

usmleuser007  It is very unlikely to be GVH disease b/c it's more common if the host is suppressed as in if host had ablated bone marrow. (FA states that it's more common with bone marrow & liver transplants) +1  
usmleuser007  any one care to explain why fibrous scars with plasma cells not a good option?... +1  


submitted by gh889(36),

Could someone please explain which drugs (if any) are at D and E?

usmleuser007  1) label D (VLDL -->ILD --> LDL) = anything that increased LPL = Fibrates which use PPAR-alpha (Rx) are good at reducing [VLDL]; therefore, less VLDL means more ILD. 2) VLDL --> fatty acid oxidation = using fats (TAGs) for energy production Here PPAR-gamma plays a role= which are Thiazolidinediones (also called glitazones) are a class of medicines that may be used for the treatment of type 2 diabetes. They are also good at reducing serum TAGs Note VLDL are very rich in TAGs +  


submitted by seagull(413),

If you don't know what Dicumarol does like any normal human. The focus on what aspirin doesn't do, namely it's doesn't affect PT time and most pills don't increase clotting (especially with aspirin). This is how I logic to the right answer.

usmleuser007  If that's then thinking, then how would you differentiate between PT & PTT? +2  
ls3076  Why isn't "Decreased platelet count" correct? Aspirin does not decrease the platelet count, only inactivates platelets. +  


submitted by mattnatomy(21),

Crackles either indicates chronic bronchitis or consolidation (from pneumonia or pulmonary edema).

Given that there's only a 1 day history of SOB, I'm leaning more towards lobar pneumonia. Maybe that's also what's causing the S3 at the LLSB? If it's Staph Aureus, I guess we could be looking at acute endocarditis + pneumonia? Or Q Fever? But that's just speculation. Could also just be that the lung consolidation is altering blood flow, leading to the back up into the Right Atrium & Ventricle.

brise  Patient has CHF from the S3 heart sound and has MR. You hear fine crackles in early congestive heart failure. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4518345/ +9  
usmleuser007  No Infection - normal temps ; Q-fever presents with A patient with exposure to waste from farm animals who develops: a. nonspecific illness (myalgias, fatigue, fever [>10 days], b. retroorbital headache) c. normal leukocyte count d. Thrombocytopenia e. increased liver enzymes +  


submitted by marbledoc(0),

Why would you ask the patient to identify the pros and cons? I don’t get the approach here!

someduck3  There was a question about this in Uworld. for *stubborn* patients who are "not ready to quit" just yet you use the motivational approach. The technique acronym is OARS: Open ended questions, Affirmation, Reflect, Summarize. +2  
yotsubato  Additionally the guy himself says "I know smoking is bad for me" Like he knows its bad, he doesnt care, but give him nicotine replacement and maybe he'll quit... +1  
usmleuser007  I didn't think nicotine replacement was a good answer choice b/c if he isn't ready to quit then why would he agree to use alternatives. +  
usmleuser007  People who smoke and are addicted like the feel of the cigs and environmental ques. Using replacements would be more challenging. The second best answer choice would have been Rx. +  
titanesxvi  why not detail the long-therm health effects of smoking? +  
seracen  @ titanesxvi: I assume because they always like the most "open ended" response. If you start detailing the long term effects, the patient might interpret that as attempting to convince, and might resist or feel pressured. By having the patient elucidate what they consider pros and cons, you allow it to be an open discussion. +  


submitted by marbledoc(0),

Why would you ask the patient to identify the pros and cons? I don’t get the approach here!

someduck3  There was a question about this in Uworld. for *stubborn* patients who are "not ready to quit" just yet you use the motivational approach. The technique acronym is OARS: Open ended questions, Affirmation, Reflect, Summarize. +2  
yotsubato  Additionally the guy himself says "I know smoking is bad for me" Like he knows its bad, he doesnt care, but give him nicotine replacement and maybe he'll quit... +1  
usmleuser007  I didn't think nicotine replacement was a good answer choice b/c if he isn't ready to quit then why would he agree to use alternatives. +  
usmleuser007  People who smoke and are addicted like the feel of the cigs and environmental ques. Using replacements would be more challenging. The second best answer choice would have been Rx. +  
titanesxvi  why not detail the long-therm health effects of smoking? +  
seracen  @ titanesxvi: I assume because they always like the most "open ended" response. If you start detailing the long term effects, the patient might interpret that as attempting to convince, and might resist or feel pressured. By having the patient elucidate what they consider pros and cons, you allow it to be an open discussion. +  


submitted by usmleuser007(110),

Vitamin E deficiency is known to cause similar spinal defects as Vitamin B12 deficiency. However, anemia is not seen.

ergogenic22  Also corticalspinal tract symptoms are not seen, but dorsal column and spinocerebellar tracts are seen +1  
sinforslide  In this case, patient's CF also predisposes fat-soluble vitamin deficiency. +2  
breis  FA pg 70 +  
usmleuser007  Correction: Read more on this Vitamin-E deficiency can in fact cause anemia - hemolytic anemia. This is b/c VitE work as an anti-oxidant; and therefore with reduced anti-oxidation RBCs are more prone to oxidative injuries. +2  


submitted by usmleuser007(110),

Confidence interval increases with decreased sample size.

usmleuser007  would require a a large sample size to see if there is a true difference +  
claptain  This question is bogus. CI does not always increase with decreased sample size or vice versa. Four readings with small variation would give a narrower CI than 10 readings with greater variation. The only thing you can be certain about by adding more samples is that the CI will most likely change, but which direction is uncertain. +  
bartolomoose  Recall the formula for 95%ci Mean +/- 1.96* (SD/sqrt(samplesize)) +  


submitted by oznefu(7),

Could anyone give an example of what diseases would best match the other answer choices?

vonhippelindau  Leprosy is a noncaseating granuloma fyi. I found that granuloma with suppuration can be caused by blastomycosis according to Robbins (pg 710): “In the normal host, the lung lesions of blastomycosis are suppurative granulomas. Macrophages have a limited ability to ingest and kill B. dermatitidis, and the persistence of the yeast cells leads to continued recruitment of neutrophils. In tissue, B. dermatitidis is a round, 5- to 15-μm yeast cell that divides by broad-based budding. It has a thick, double-contoured cell wall, and visible nuclei (Fig. 15-38). Involvement of the skin and larynx is associated with marked epithelial hyperplasia, which may be mistaken for squamous cell carcinoma.” +  
usmleuser007  Pyogranulomatous Inflammation An inflammatory process in which there is infiltration of polymorphonuclear cells into a more chronic area of inflammation characterized by mononuclear cells, macrophages, lymphocytes and possibly plasma cells. Actinomyces sp. is gram-positive, acid-fast–negative filamentous bacteria that cause pyogranulomatous infections in dogs, cats, cattle, goats, swine, horses, foxes and human beings. +  


submitted by hungrybox(216),

Following a stroke, this patient had weakness of her left face and body, so the stroke must have affected the right side of her brain. B was the only choice on the right side of her brain.

Still confused? Read on...

The voluntary motor fibers (corticospinal tract) descend from the primary motor cortex, cross (decussate) at the medullary pyramids, and then synapse at the anterior motor horn of the spinal level.

Because of decussation at the medullary pyramids, you should make a note of where any stroke occurs. Is it above the medullary pyramids? Then it will affect the side opposite the stroke (contralateral). Is it below the medullary pyramids? Then it will affect the same side as the stroke (ipsilateral).

hungrybox  Woops, E is also on the right side (also remember that imaging is looking up at someone, feet first). But a cerebellar stroke would have caused ataxia. +  
mnemonia  Very nice!! +  
usmleuser007  What gets me is that they mention that Left 2/3 of face is affected. This should indicate a non cortical innervation as most of the cranial nuclei are bilaterally innervated from the left and right hemisphere. If left 2/3 of the face is affected then it should also mean that the lesion is after CN5 nuclei. +1  
yotsubato  @hungrybox Thats not the cerebellum thats the occipital lobe. You would see leftsided homonymous hemianopsia in that lesion +  
mrsmac  To my mind, it is simpler to consider the question first in terms of blood supply distribution. Left sided hemiparesis and weakness of lower 2/3 of face are both indicative of a MCA rupture/stroke (First Aid 2018 pg. 498). Furthermore, since the injury has affected motor function we would be considering the descending tract i.e. lateral corticospinal which courses through the ipsilateral posterior limb of the internal capsule then decussates in the caudal medulla. +1  
mrsmac  You're considering the wrong CN here. CN5 motor function involves muscles of mastication and lower 2/3 of tongue. The nerve in question in this case is CN7/VII Facial n. CNVII UMN injury affects the contralateral side, whereas LMN injury affects ipsilateral (First Aid 2018 pg. 516). i.e. before and after the nucleus in pons respectively. I hope this helps. +1  
nala_ula  Spastic means UMN lesion, since they also don't specify if there is arm or leg weakness, I didn't assume it was MCA stroke. I went with the reasoning that for there to be spastic hemiparesis, there must be damaged to the UMNs and therefore the internal capsule is where these tracts are. +  
champagnesupernova3  Omg this whole discussion is confusing. Internal capsule contains ALL corticospinal and corticobulbar fibers = contralateral hemiparesis and UMN facial lesion +  


submitted by mcl(202),

Methionine is an essential amino acid. All others listed are not.

scalpelofthenorth  Pg 81 Tyrosine is listed as an essential AA. Should be tryptophan for those who got this wrong like me. +  
neonem  But tyrosine can come from phenylalanine, so it's not really essential right? +  
gh889  in FA2019, it is listed as Tryptophan, not Tyrosine. That was corrected. +1  
usmleuser007  Note: Tyrosine is ONLY essential with PKU in children +  
niboonsh  bro FA2018 lists tyrosine as an essential AA. They played us. +1  


submitted by nosancuck(34),

Yo dawg we all about PVT TIM HaLL

Phenylalanine, Valine, TryptoDANK, Threonine, Isoleucine, Methionine, Histidine, Leucine Lysine

meningitis  I don't understand what the question is asking... can someone please explain it to me? Patient doesnt eat protein, shes chubby. What does methionine have to do with this? +2  
charcot_bouchard  Just basically asking which is essential amino acids. +1  
usmleuser007  Essential amino acids (something i came up with) 1. "Three HAL fans will try meth" a. Threonine = Three b. Histidine; Arginine; Lysine = HAL c. Phenylalanine = fans d. Valine; Isoleucine; Leucine = will e. Tryptophan = try f. Methionine = meth +1  
nala_ula  They're saying there is a lack of good quality protein -> slight nutritional deficiency. She may have acquired weight but it's not because of protein. So they're specifically asking what amino acid she might be missing due to her subpar diet. Since essential amino acids are those that the body cannot make itself, out off those listed, methionine is the essential amino acid. It's on page 81 of FA 2019. +6  
nala_ula  correct me if I'm wrong please :) +  
hello  For anyone confused trying to follow @usmleuser007's comment -- slightly modified Essential amino acids mnemonic "Ah, Three fans will try meth" Ah = arginine, histidine Three = Threonine Fans (phans)= Phenylalanine Vil (Will -- German accent pronouncing English word 'will') = valine, isoleucine, leucine, lysine Try = tryptophan Meth = Methionine +  


submitted by hungrybox(216),

Dysplastic nevi are a precursor to melanoma. They have irregular, "dysplastic" borders. Remember the "B" in ABCD stands for irregular Borders. Nevus means mole.

Other answers:

  • acanthosis nigricans - Darkening of skin associated with Type II diabetes mellitus

  • basal cell carcinoma of skin - Rarely, if ever metastasizes. Commonly affects upper lip.

  • blue nevus - Blue-colored type of common mole. Benign.

  • pigmented seborrheic keratosis - "Stuck on" appearance. Mostly benign. Affects older people.

  • (Note - you usually see only one. If multiple seborrheic keratoses are seen, it indicates a GI malignancy - aka "Leser-Trélat sign)
usmleuser007  correction ~ BCC affects the lower lip more than the upper +  
sympathetikey  Pathoma says upper lip, good sir +6  
hungrybox  Yeah basal cell carcinoma actually affects the upper lip. Counterintuitive because it's "basal" which seems to go along with the lower lip. Here's another source (this website is fucking gold btw): https://step1.medbullets.com/oncology/121593/basal-cell-carcinoma-of-the-skin +2  


submitted by hajj(0),

can anyone explain this? i know median for y is higher by calculation but x has two modes so how come y has higher mode?

lispectedwumbologist  The mode in X is 32 and the mode in Y is 80 +  
lispectedwumbologist  The mode in X is 70 and the mode in Y is 80* +1  
hajj  Thank you! +  
hungrybox  Just checking in so I could feel smart about getting this right despite bombing the rest of the test lmao +2  
usmleuser007  can someone please explain the median in this +  
nala_ula  The median can be known by first assembling the numbers in order from least to greater. If it's an uneven number set, the number in the middle is the median (for example: 4, 10, 12, 20, 27 = median is 12 since this is the number in the middle); if the numbers are even then you have to take the two values in the middle, add them up and divide them by 2 [for example: 4, 10, 12, 12, 20, 27 = (12+12)/2 = 12]. Page 261 on FA 2019 explains it as well. Not sure if I explained it well... good luck on the test, people! +  
dubin johnson  Can someone please explain how the mode for Y than X. Not sure how we got the values above. Thanks! +  
dubin johnson  I mean how is the mode for Y greater than mode for x? +1  
sgarzon15  Mode is the one that repeats the most once you list them in order +  
usmile1  Median would be the BP value that the person in the 50th percentile of each group would have. So for group X, to find the 50th percent value, I added 8 + 12 + 32 = 52, which is right above 50, so the median would be 70 mmHg for group X. Doing the same thing for group Y, 2+8+10+20+ 18 = 58; the 50th percentile would fall in group that had a BP of 90 mmHg. which makes the median higher for group Y. hope that isn't wrong, and helps someone! +4  


submitted by moneysacs(0),

Why is does a PDA after birth result in "higher than normal left ventricular cardiac output" over increased "right ventricular PO2"? Does the pulm artery --> aorta shunt become reversed after birth, so higher oxygen aorta blood would flow back into the right ventricle? I get that more blood would be pumped to the left ventricle, resulting in RVH/LVH, but don't understand the O2 bit.

usmleuser007  1) higher than normal CO b/c blood is shunted from aorta to pulmonary arteries. This blood is added to the volume that was pumped into the pulmonary arteries by the RV. Now when the oxygenated blood returns to the LA & LV, the O2 content would be greater d/t higher blood volume. Also for that same reason more blood is returning to the LV (d/t LV volume plus fraction of RV volume). This increased the CO. Right--> Left shunts have late cyanosis b/c the RV is pushing against the excess pressure generated by the LV. This leads to Eisenmenger Syndrome as RV enlarges and pushes against the pressure from the LV in the PDA. Thus shifting Left to right to right to Left and thus the late cyanosis +1  
temmy  The anatomy is aorta-pulmonary artery-pulmonary veins-left atrium-left ventricle Notice that the blood did not come across the right heart at all and because of the LEFT TO RIGHT shunt of the PDA, we add more volume to the LEFT side. Hence the increased left ventricular output +2  


"Upon application of pressure to the internal end of the cervix, oxytocin is released (therefore increase in contractile proteins), which stimulates uterine contractions, which in turn increases pressure on the cervix (thereby increasing oxytocin release, etc.), until the baby is delivered.

Sensory information regarding mechanical stretch of the cervix is carried in a sensory neuron, which synapses in the dorsal horn before ascending to the brain in the anterolateral columns (ipsilateral and contralateral routes). Via the median forebrain bundle, the efferent reaches the PVN and SON of the hypothalamus. The posterior pituitary releases oxytocin due to increased firing in the hypothalamo-hypophyseal tract. Oxytocin acts on the myometrium, on receptors which have been upregulated by a functional increase of the estrogen-progesterone ratio. This functional ratio change is mediated by a decrease in myometrial sensitivity to progesterone, due to an increase in progesterone receptor A, and a concurrent increase in myometrial sensitivity to estrogen, due to an increase in estrogen receptor α. This causes myometrial contraction and further positive feedback on the reflex.[1]"

https://en.wikipedia.org/wiki/Ferguson_reflex

seagull  https://www.ncbi.nlm.nih.gov/pubmed/8665768 a counter argument for PGE if you chose that answer. However, the author believes oxytocin is superior. +  
usmleuser007  1) PGE rises initially that causes the uterine contractions= this would be equivalent to when someone say #of contractions per time period. 2) Oxytocin is increased when the cervix is manipulated (ie. the birth canal reflex). +2  


Legionella is common causes of pneumonia superimposed on chronic obstructive pulmonary disease.

asapdoc  Im pretty sure so is strept pneumoniae +2  
usmleuser007  COPD is also exacerbated by Viral infection: Rhinovirus, influenza, parainfluenza; and Bacterial infection: Haemophilus influenzae, Moraxella catarrhalis, Streptococcus. however, the questions gives a hint that it may be legionella = "weekend retreat" which may be associated with this infection +  
loopers  From FA 2017 pg 139: Legionnaires’ disease—severe pneumonia (often unilateral and lobar A ), fever, GI and CNS symptoms. Common in smokers and in **chronic lung disease.** +1  
kentuckyfan  I also believe that the other attendees showed signs of pontiac fever, which is another hint they tried to get at. +1  
luke.10  i did it wrong and chose influenza virus since it is most common infection in COPD but the clue in the Question is that the other attendee didnt get sick since in legionella there is no person to person transmission +  
endochondral   but in Uworld s. pneumo is one of the most common bacterial exacerbation of COPD legionella wasn't even mentioned. How do we rule out s. pneumo ? +1  
nala_ula  maybe because in children s.pneumo causes otitis media? +  
smc213  Another hint made in the Q stem is the location being rural Pennsylvania.... Legionnaires disease was first discovered by the outbreak in 1976 at a convention held in Philadelphia, Pennsylvania. Not sure why I know this fact... +  
hpsbwz  Biggest hint towards legionella to me was that they all were at a residence hall... i.e. where there'd be air conditioners and such. +1  


submitted by hayayah(394),

Patient has chronic diarrhea leading to metabolic acidosis. Respiratory compensation will lead to decreased CO2 (respiratory alkalosis via hyperventilation).

usmleuser007  Aldo would increase b/c protons are anti-transported with potassium --> leads to hyperkalemia --> aldo activation ADH will also increase b/e of volume loss +  


submitted by neonem(251),

Obstructive uropathy causes a postrenal azotemia --> when prolonged, tubular damage ensues. This leads to an acute tubular necrosis, characterized by necrotic plugs in the tubular system as seen in the image

meningitis  Does anyone know the relevance of the stem saying: "during this time she also has been crying frequently"? +5  
usmleuser007  Think the postrenal azotemia is d/t her pregnancy. With the increasing in size fetus, the pelvic cavity is being compressed and thus there is pressure on the ureters. This leading to the presentation. As per above --- the crying maybe just d/t her pain and emotional stress caused by worrying about possible complications regarding her fetus. +2  
maxillarythirdmolar  My gut tells me it must be some sort of transient change in placental size with hormonal changes. It's reminiscent of what you might expect for breast changes during the menstrual cycle, imo +  


submitted by usmleuser007(110),

https://www.ncbi.nlm.nih.gov/pubmed/301658

Relief of intractable pain was produced in six human patients by stimulation of electrodes permanently implanted in the periventricular and periaqueductal gray matter. The level of stimulation sufficient to induce pain relief seems not to alter the acute pain threshold. Indiscriminate repetitive stimulation produced tolerance to both stimulation-produced pain relief and the analgesic action of narcotic medication; this process could be reversed by abstinence from stimulation. Stimulation-produced relief of pain was reversed by naloxone in five out of six patients. These results suggest that satisfactory alleviation of persistent pain in humans may be obtained by electronic stimulation.

usmleuser007  These questions seem unfair to test because they are based on experimental data. Guess they are there to limit a perfect score. +  
xxabi  I just read it as patients take opioids to blunt or control pain. So if the electrode does the same thing (decrease pain), then an antagonist of opioids (naloxone) would bring the pain back? Idk if that reasoning is sound but that's the logic I used, I didn't even think of it as experimental. +4  
xxabi  Also its the only one that's an opioid antagonist from the list! +1  
redvelvet  they are writing these questions in an evidence-based manner because the questions in medicine cannot be produced by a self imagination or logic. But that doesn't mean that we have to know their exact evidence like this question. we can use our own basic knowledge and adjust it with logic. so opioids have an analgesic effect in the body and naloxone can revert it. +1  
champagnesupernova3  Anything that reduces pain by brain stimulation is increasing endogenous opiods like endorphins and encephalitis. +  
champagnesupernova3  Enkephalins* not encephalitis +  


usmleuser007  in a per-protocol analysis,[6] only patients who complete the entire clinical trial according to the protocol are counted towards the final results +1  
sympathetikey  "In an ITT population, none of the patients are excluded and the patients are analyzed according to the randomization scheme." +1  
smc213  This video helps https://www.youtube.com/watch?v=Kps3VzbykFQ +2  
rio19111  Thx smc213, really helped. +  


submitted by thomas(3),

Not sure about this, but it seems to me that this is referring to "pseudocholinesterase inhibitor deficiency. It's an enzyme defect that is triggered by NMJ blockers - succinylcholine or curare's.

https://en.wikipedia.org/wiki/Pseudocholinesterase_deficiency

usmleuser007  I believe this question was stating that AchE activity was abnormal = it was not lowering the Ach activity. Which suggests that another ligand like Ach was being used. +