to snoo-finity ... and beyond!
to snoo-finity ... and beyond!
other answers:
inhibition of H2 receptors: (for GERD) prevent gastric acid secretion (cimetidine,
inhibition of phosphodiesterases (PDE):
β2 agonists: (for asthma) cause bronchodilation
(idk lymphocyte membrane stabilization)
Macroscopically, squamous cell carcinoma tends to be off-white in color, arising from, and extending into a bronchus.
Source: Radiopedia
when diff single strand repair mechanisms are used:
ATII constricts the efferent arteriole. ACE inhibitors block the ACE-mediated conversion of ATI to ATII.
My impression of Amphotericin B is that it's the BIG GUNS. It straight up attacks the sterols in the fungi plasma membrane.
Meanwhile lil bitch drugs like -azoles just inhibit sterol synthesis. (-terbinafine X lanosterol, -azoles X ergosterol)
Fungins X cell wall synthesis, flucytosine X nucleic acid synthesis.
Hydrochlorothiazide is a thiazide diuretic => thiazide diuretics are associated with hypokalemia.
What other diuretics are associated with hypokalemia? Loop diuretics.
Why?
Inhibition of Na+ reabsorption occurs in both loop diuretics (inhibit NKCC cotransporter) and thiazide diuretics (inhibit NaCl cortransporter). All of this increased Na+ increases Aldosterone activity.
Relevant to this problem, Aldosterone upregulates expression of the Na+/K+ ATP antiporter (reabsorb Na+ into body, expel K+ into lumen). This results in hypokalemia in the body.
Hang on, there's more high yield info!
Aldosterone does one other important thing - activation of a H+ channel that expels H+ into the lumen.
So, given that this patient has hypokalemia, you know there is upregulation of Aldosterone. Do you think her pH would be high, or low? Exactly, it would be high because inc. Aldosterone => inc. H+ expelled into the lumen => metabolic akalosis.
Now you understand why both loop diuretics and thiazide diuretics can cause what's called "hypokalemic metabolic alkalosis."
Great video I used to learn this material.
Loop diuretics are first line for acute congestive heart failure. That should help you remember that they are the most potent diuretics, so they're often used in the acute treatment of edema.
Loperamide: Agonist at u-opioid receptors. Slows gut motility (remember, constipation is a common side effect for all opioids).
quiz yourself:
Q: Would a junkie want to use Loperamide?
A: No, it has poor CNS penetration (which is why it has a low addictive potential).
Q: Would a junkie rather have morphine or buprenorphine?
A: Morphine. Both are u-opioid agonists, but morphine is a full agonist while buprenorphine is only a partial agonist.
Q: What about morphine vs. codeine?
A: Trick question, both are partial agonists.
HIGH YIELD: "nonbilous vomiting" means that the issue/obstruction comes before (proximal to) the second duodenum, where bile is released.
At around ~4 weeks (give or take a few) is when pyloric stenosis usually shows up.
ez pts for u now keep it up
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).
The anatomic snuffbox is formed by the tendons of the extensor pollicis brevis, the abductor pollicis longus, and the extensor pollicis longus. (figure)
The floor is formed by the scaphoid bone, and it is here that one can palpate for a possible fractured scaphoid.
Source: Gray's Anatomy Review
quiz yourself answers:
This video explains genital embryology extremely well.
If you felt totally lost like me, watch the video first at 2x, then check out the bottom figure on pg. 608 in FA 2019.
Relevant to this question:
Quiz yourself (answers in a separate post):
jugular venous distention = left heart failure
pulmonary edema = right heart failure
Four-chamber dilation is the most likely answer.
Other answers:
preeclampsia presents differently:
The 2 commandments of ethics questions:
Served me well on this question.
Huntington's disease
Remember "HUNT 4 an animal, put it in a CAGe". Huntingtin gene found on Chromosome 4. CAG is the trinucleotide repeat:
Wernicke-Korsakoff syndrome due to thiamine (B1) deficiency. Common in alcoholics.
The reason why they said "results of alcohol and drug screen are negative" is that the differential includes acute alcohol intoxication.
Wernicke's triad:
*presents here as nystagmus
Korsakoff's psychosis:
/u/cantaloupe5 had a great explanation.
Here's an image of the different stages following myocardial infarction. Note the "contraction bands" are what define coagulative necrosis.
why hemolysis is wrong:
There should almost never be straight up bilirubin in the urine. In hemolysis, the excess bilirubin is excreted in the bile. After bacterial conversion and reuptake, some will be excreted in the urine as urobilin. However, in obstructive disorders, the conjugated bilirubin will never have the opportunity to undergo bacterial conversion to sterco/urobilin. In this way, the conjugated bilirubin has no other way to be excreted other than directly in the urine.
credits to /u/alacran763 on reddit
According to the USMLE, selenium's only use is in selenium sulfide as a treatment for a fungus called Malassezia spp (Tinea versicolor).
some wrong answers:
*makes sense b/c myeloblasts are precursors to granulocytes, which use MPO to fight off infections
Long answer ahead, but bear with me.
HINT: v looks kind of like y, whereas k looks more like x.
y-intercept = 1/Vmax
x-intercept = 1/Km
Note that Vmax, as a measure of performance, can be altered through many things. Meanwhile, Km is a set characteristic of the enzyme, and cannot be altered.
In this example, the enzyme performance (Vmax) is increased by increasing the vitamin cofactor so that it reaches a "normal" activity. However, the enzyme is still inherently shitty due to a congenital defect, so the Km stays the same.
ethambutol = EYEthambutol
Great mnemonic for remembering that EYEthambutol is the component that causes visual problems in RIPE therapy for TB.
other answers:
hypnoGO to sleep = night time hallucinations
paroxysmal nocturnal dyspnea: PNH is a hemolytic anemia. No signs of hemolytic anemia (hematuria, jaundice, dec. haptoglobin).
sleep apnea: Associated with obesity, loud snoring.
Due to glycine's small size, it creates "kinks" in the amino acid sequence. These kinks are needed to correctly form the secondary structure.
Other answers:
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.
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.
jugular venous distention = left heart failure
pulmonary edema = right heart failure
Four-chamber dilation is the most likely answer.
Other answers:
Direct Antiglobulin = Direct Coombs Test
Detects antibodies bound directly to RBCs. Hemolysis most likely due to something in the transfused blood (not sure why it took 4 weeks when Type 2 HS is supposed to be quicker but w/e).
Patient most likely has Tay-Sachs disease. This figure nicely shows the biochemical pathway. Recall that both Tay-Sachs and Neimann Pick disease present with a cherry red spot on fundoscopy, but Tay Sachs lacks the hepatosplenomegaly seen in NP.
PDA flows from aorta to pulmonary artery decreasing afterload. Therefore cardiac output increases
Anyone have an idea why the decreased arterial O2 saturation is incorrect? Assuming she has pulm edema since she has LE edema, wouldn't a lower O2 sat be expected too?
This question is describing terminal insomnia, which is common either in MDD or normal aging. Out of those two MDD is the only thing in option choice. Plus, old age is a risk factor for MDD.
Even though the question does not describe 5 symptoms needed to diagnose MDD, MDD is the only logical choice.
other answers:
inhibition of H2 receptors: (for GERD) prevent gastric acid secretion (cimetidine,
inhibition of phosphodiesterases (PDE):
β2 agonists: (for asthma) cause bronchodilation
(idk lymphocyte membrane stabilization)
Patient most likely has Tay-Sachs disease. This figure nicely shows the biochemical pathway. Recall that both Tay-Sachs and Neimann Pick disease present with a cherry red spot on fundoscopy, but Tay Sachs lacks the hepatosplenomegaly seen in NP.
Hydrochlorothiazide is a thiazide diuretic => thiazide diuretics are associated with hypokalemia.
What other diuretics are associated with hypokalemia? Loop diuretics.
Why?
Inhibition of Na+ reabsorption occurs in both loop diuretics (inhibit NKCC cotransporter) and thiazide diuretics (inhibit NaCl cortransporter). All of this increased Na+ increases Aldosterone activity.
Relevant to this problem, Aldosterone upregulates expression of the Na+/K+ ATP antiporter (reabsorb Na+ into body, expel K+ into lumen). This results in hypokalemia in the body.
Hang on, there's more high yield info!
Aldosterone does one other important thing - activation of a H+ channel that expels H+ into the lumen.
So, given that this patient has hypokalemia, you know there is upregulation of Aldosterone. Do you think her pH would be high, or low? Exactly, it would be high because inc. Aldosterone => inc. H+ expelled into the lumen => metabolic akalosis.
Now you understand why both loop diuretics and thiazide diuretics can cause what's called "hypokalemic metabolic alkalosis."
This is one of those questions I was never going to get. It's not in FA, I don't think I've seen it in class.
they're talking about a splenorenal shunt procedure
https://my.clevelandclinic.org/health/treatments/4950-distal-splenorenal-shunt
Catheter placement:
https://aneskey.com/wp-content/uploads/2016/08/image00804.jpeg
Recall that the lung apex extends above the first rib.
This occurred within 6 hours and caused some pulmonary edema and respiratory distress after a transfusion caused by the donor's anti-leukocyte antibodies just destroying the recipients neutrophils and respiratory endothelial cells.
while allergic/anaphylaxis can cause respiratory arrest and shock it has a somewhat different picture, no wheezing, itchiness or whatever and according to first Aid it happens within minutes to 2-3 hours which is at least double what we're seeing here. also beware of IgA deficient people in this choice.
PE, eh I don't think it affects Pao2 that often much according to this super duper high yield resource. but uhh yeah doesn't feel PE kinda question https://emedicine.medscape.com/article/300901-workup#c12
pneomina, right after all the infusion business and no mention of fever or anything? Nah.
go to page 114 of first aid. I'm pretty sure we need to know our infusion/transplant crap because it just keeps coming up in uworld but this whole exam is a crapshoot.
Forgive me if I made a mistake/wrong about anything, I mostly got info from first aid. plz correct if there is a mistake, good luck.
This occurred within 6 hours and caused some pulmonary edema and respiratory distress after a transfusion caused by the donor's anti-leukocyte antibodies just destroying the recipients neutrophils and respiratory endothelial cells.
while allergic/anaphylaxis can cause respiratory arrest and shock it has a somewhat different picture, no wheezing, itchiness or whatever and according to first Aid it happens within minutes to 2-3 hours which is at least double what we're seeing here. also beware of IgA deficient people in this choice.
PE, eh I don't think it affects Pao2 that often much according to this super duper high yield resource. but uhh yeah doesn't feel PE kinda question https://emedicine.medscape.com/article/300901-workup#c12
pneomina, right after all the infusion business and no mention of fever or anything? Nah.
go to page 114 of first aid. I'm pretty sure we need to know our infusion/transplant crap because it just keeps coming up in uworld but this whole exam is a crapshoot.
Forgive me if I made a mistake/wrong about anything, I mostly got info from first aid. plz correct if there is a mistake, good luck.
hit me up wit dat HNPCC boi! all abou dat LYNCH SYNDROME
under 8 years old for girls is a bad sign, 8 is okay. under 9 for boys is a bad sign.
just watch out for any 6 year old or something like that. beware of that GnRH either centrally or some some other source. -first aid 2019 pg 623
It said it was fatal to males in utero, and the question asked about live born offspring. Since the males aren’t being born in the first place, I said 50% females and 0% males.
Bruh let me tell you a lil secret
PEEP prevents Atelectasis AKA dat LUNG COLLAPSE
Dont be worryin about random words they puts in front of the HIGH YIELD ones
If anybody has a good way of distinguishing/remembering all the different presentations for genital sores, I'd appreciate the help.
This is a case of acute gout. Monosodium urate crystals are taken up by neutrophils, leading to an acute inflammatory reaction. T-cells aren't really involved in gout (more rheumatoid arthritis).
Great video I used to learn this material.
This has been a tough concept for me to get, but I think I'm finally there:
The stem is describing primary adrenal insufficiency, or Addison's.
don't be a dick? not really sure what more there is to it. The patient doesn't have any other family so this woman should be considered family
The cervix is the only structure that would result in bilateral blockade.
I know this is just a straight up fact from FA, but couldn't ureters (transitional cell carcinoma) also be correct?
This one was tricky but I think you could’ve done this one without knowledge of NMDA receptors. Stem told you that glutamate activates both non-NMDA and NMDA receptors but it activated only non-NMDA receptors in the early phase. That means NMDA receptors activate after non-NMDA receptors. That means something was delaying NMDA receptor activating and the only answer that made sense as the Mg inhibiting NMDA at resting potential. Once the cell is depolarized by non-NMDA receptors, NMDA receptors can be activated.
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).
Vasoconstriction (narrowing of a tube) will cause the flow rate to increase through that tube, which decreases radial/outward pressure. The faster a fluid moves through a tube, the less “outward” force it exerts. (This is known as the Venturi effect.)
The anatomic snuffbox is formed by the tendons of the extensor pollicis brevis, the abductor pollicis longus, and the extensor pollicis longus. (figure)
The floor is formed by the scaphoid bone, and it is here that one can palpate for a possible fractured scaphoid.
Source: Gray's Anatomy Review
The anatomic snuffbox is formed by the tendons of the extensor pollicis brevis, the abductor pollicis longus, and the extensor pollicis longus. (figure)
The floor is formed by the scaphoid bone, and it is here that one can palpate for a possible fractured scaphoid.
Source: Gray's Anatomy Review
aka ampulla of Vater or the hepatopancreatic duct
Note: The abducens n. is actually the nerve most likely to be damaged by an expanding internal carotid aneurysm in the cavernous sinus but they give you specific CN3 function in this question.
Ok I get that if 500 already have the disease then the risk pool is dropped to 2000 students but the question specifically says that the test is done a year later...if 500 people had chlamydia, you would treat them. You don't become immune to chlamydia after infection so they would go back into the risk pool, meaning the pool would return to 2500. The answer should be 8%, this was a bad question.
Anyone have an idea why the decreased arterial O2 saturation is incorrect? Assuming she has pulm edema since she has LE edema, wouldn't a lower O2 sat be expected too?
AV Fistulas re-rout blood from the arterial system to the venous system, by-passing the Arterioles = Increase PL ---> INCREASE VR. All in all = Increase CO.
According to UWorld, the arterioles are a major source of resistance ... so bypassing the arterioles results in a decrease in Total Peripheral Resistance ... causing an increase in the rate and volume of blood returning to the heart. I am pretty sure there is more to the physiology behind this, but I hope this explained a little.
Idiotypic means --- antibody against antibody. B cells don't have surface antibodies but mere synthesize them.
Idiotypic means --- antibody against antibody. B cells don't have surface antibodies but mere synthesize them.
I think the concept they’re testing is the increased TBG levels in pregnancy, and not just hyperthyroidism in general.
When screening for hypo/hyperthyroidism, TSH levels are ALWAYS preferentially checked because they are more sensitive to minute differences in T3/T4. Often times TSH levels can demonstrate a change even when T3/T4 levels are in the subclinical range. The only exception to this would be in pregnancy (and I guess maybe liver failure? I doubt they would ask this though). High estrogen levels prevents the liver from breaking down TBG, leading to increased TBG levels in the serum. This binds to free T4, decreasing the amount of available free T4. As a compensatory mechanism, TSH levels are transiently increased and the RATE of T4 production is increased to replenish baseline free T4 levels. However the TOTAL amount of T4 is increased.
The question is asking how to confirm hyperthyroidism in a pregnant woman --> you need to check FREE T4 levels (because they should be normal due to compensatory response). You cannot check TSH (usually elevated in pregnancy to compensate for increased TBG), and you cannot check total T4 levels (will be increased). You got the answer right either way but I think this is a different reasoning worth considering, because they can ask this concept in other contexts of hyper-estrogenism, and if they listed “TSH” as an answer choice that would be incorrect.
the majority of carbon dioxide molecules are carried as part of the bicarbonate buffer system. In this system, carbon dioxide diffuses into the RBCs. Carbonic anhydrase (CA) within RBCs quickly converts the carbon dioxide into carbonic acid (H2CO3). Carbonic acid is an unstable intermediate molecule that immediately dissociates into bicarbonate ions (HCO3-) and hydrogen (H+) ions.
The newly synthesized bicarbonate ion is transported out of the RBC into the plasma in exchange for a chloride ion (Cl−); this is called the chloride shift. When the blood reaches the lungs, the bicarbonate ion is transported back into the RBC in exchange for the chloride ion. The H+ ion dissociates from the hemoglobin and binds to the bicarbonate ion. This produces the carbonic acid intermediate, which is converted back into carbon dioxide through the enzymatic action of CA. The carbon dioxide produced is expelled through the lungs during exhalation.
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?
I might be the only person on earth who got this one wrong, but regardless:
"ITT analysis includes every subject who is randomized according to randomized treatment assignment. It ignores noncompliance, protocol deviations, withdrawal, and anything that happens after randomization."[1]
Orchiectomy = ↓ testosterone production = ↓ DHT => prostate cells undergo apoptosis. (This mechanism is similar to using 5α-reductase blockers to treat BPH.)
Apoptosis is characterized by DNA fragmentation (pyknosis, karyorrhexis, karyolysis).
ethambutol = EYEthambutol
Great mnemonic for remembering that EYEthambutol is the component that causes visual problems in RIPE therapy for TB.
Candida is a part of the normal flora of skin, could cause contamination of a central venous catheter. The question states that the organism is purple, budding, did not respond to broad spectrum antibiotics (aka they didn't use fluconazole or amphotericin B). Lastly, they showed it plated on blood agar and there was no hemolysis which eliminates staph (the only other possible contender here.)
Cryptococcus usually involves meningitis in immunocompromised pts. E. coli is gram negative sporothrix is usually transmitted by a thorn on a rose or someone with a history of gardening
Here’s one way to process-of-eliminate “decreased hydrogen-bond formation”: I’m not a big fan of this line of reasoning, but technically alanine as a side group has more hydrogens* for potential hydrogen bonding than glycine:
alanine: —CH3
glycine: —H
So, “technically,” alanine would permit more hydrogen-bond formation, which might allow you to eliminate that choice.
That said, it seems almost impossible to rule out (without very technical knowledge or some provided experimental data) that the slightly larger alanine does not impair hydrogen bonding between collagen molecules via steric (spatial) interference. In simpler terms, since alanine is larger, you would think that it must somehow interfere with the hydrogen-bonding that occurs with the wild-type glycine.
---
*Strictly speaking, it’s not the number of hydrogens but also the strength of the dipole that facilitates hydrogen bonding: a hydrogen bound to a strongly electronegative molecule like fluorine will “appear” more positive and, thus, hydrogen-bond more strongly with a nearby oxygen (compared with a hydrogen connected to carbon, for example).
Further reading:
Membranous Glomerulonephritis is Nephrotic; ONLY PROTEINURIA is in the vignette
It can't be MPGN because MPGN is Nephritic with possible Nephrotic
Other choices are eliminated by Renal Biopsy
So... theoretically an isolated decrease in HR would increase CO due to inc. preload, right?
But CO decreases in this case b/c the effect of inc. TPR is more powerful?